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Journal articles on the topic 'ENVIRONMENTAL EXPOSURE PATHWAY'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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1

López-Gálvez, Wagoner, Quirós-Alcalá, Horne, Furlong, Avila, and Beamer. "Systematic Literature Review of the Take-Home Route of Pesticide Exposure via Biomonitoring and Environmental Monitoring." International Journal of Environmental Research and Public Health 16, no. 12 (June 19, 2019): 2177. http://dx.doi.org/10.3390/ijerph16122177.

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Background: Exposure to pesticides via take-home can be an important pathway for farmworkers' families. Objective: The aim of this review was to summarize and analyze the literature published during the last decade of exposure to pesticides via take-home pathway in farmworkers' families. Methods: We conducted a systematic review to identify peer-reviewed articles of interest; only articles related to take-home pathway that included some sort of pesticide monitoring were considered for inclusion. Systematic reviews, literature reviews, and meta-analyses were excluded, resulting in a total of 39 articles elected for analysis. The articles were summarized based on the location of the study, population (sample size), pesticide analyzed, and type of sample. Results: The majority of the reviewed studies were conducted in the U.S., but there seems to be an increase in literature on pesticide take-home pathway in developing countries. Most of the articles provided evidence that farmworkers’ families are exposed to pesticides at higher levels than non-farmworkers’ families. The levels may depend on several factors such as seasonality, parental occupation, cohabitation with a farmworker, behavior at work/home, age, and gender. Community-based interventions disrupting the take-home pathway seem to be effective at reducing pesticide exposure. Discussion/Conclusion: The take-home pathway is an important contributor to overall residential exposures, but other pathways such as pesticide drift, indoor-residential applications, and dietary intake need to be considered. A more comprehensive exposure assessment approach is necessary to better understand exposures to pesticides.
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2

Wright, Jackie, Bob Symons, Jonathon Angell, Kirstin E. Ross, and Stewart Walker. "Current practices underestimate environmental exposures to methamphetamine: inhalation exposures are important." Journal of Exposure Science & Environmental Epidemiology 31, no. 1 (September 1, 2020): 45–52. http://dx.doi.org/10.1038/s41370-020-00260-x.

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AbstractCurrent practice for determining the exposure to methamphetamine in contaminated homes relies on the analysis of surface wipe sample to address direct contact exposures. The movement of methamphetamine into the air phase, and the potential for inhalation exposures to occur within residential homes contaminated from former clandestine manufacture or smoking of methamphetamine has been generally poorly characterised and understood. All available risk-based guidelines for determining safe levels of methamphetamine in residential properties do not include any consideration of the inhalation pathway as an exposure route. This study showed that methamphetamine can readily move from contaminated materials in a home into the air phase. This movement of methamphetamine into the air phase provides both an exposure pathway and a mechanism for the transfer of methamphetamine throughout a property. The inhalation exposure pathway has the potential to result in significant intake of methamphetamine, adding to dermal absorption and ingestion exposure routes. Guidelines that are established for the assessment of methamphetamine contaminated properties that ignore inhalation exposures can significantly underestimate exposure and result in guidelines that are not adequately protective of health. This study also demonstrates that sampling methamphetamine in air can be undertaken using commercially available sorption tubes and analytical methods.
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Hattemer-Frey, Holly A., and Curtis C. Travis. "Benzo-a-Pyrene: Environmental Partitioning and Human Exposure." Toxicology and Industrial Health 7, no. 3 (May 1991): 141–57. http://dx.doi.org/10.1177/074823379100700303.

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A multimedia transport model was used to evaluate the environ mental partitioning of benzo-a-pyrene ( BaP) . Measured and pre dicted environmental concentrations were used to estimate the accumulation of BaP in the food chain and the subsequent ex tent of human exposure from inhalation and ingestion. Results show that BaP partitions mainly into soil ( 82%) and sediment ( 17%) and that the food chain is the dominant pathway of hu man exposure, accounting for about 97% of the total daily in take of BaP. Inhalation and consumption of contaminated water are only minor pathways of human exposure. The long-term av erage daily intake of BaP by the general population of the U. S. is estimated to be 2.2 micrograms (μ g) per day. Cigarette smok ing and indoor activities do not substantially increase human ex posure to BaP relative to exposures to background levels of BaP present in the environment. Since the increased lifetime risk as sociated with human exposure to background levels of BaP is 3.5 x 10-4, we conclude that ingestion of food items contami nated with BaP may pose a serious health threat to the U. S. population.
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Tan, Yu-Mei, Jeremy A. Leonard, Stephen Edwards, Justin Teeguarden, and Peter Egeghy. "Refining the aggregate exposure pathway." Environmental Science: Processes & Impacts 20, no. 3 (2018): 428–36. http://dx.doi.org/10.1039/c8em00018b.

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Ho, John W., and Alex W. Ho. "Environmental lead exposure induces changes in the heme biosynthetic pathway." Environmental Toxicology and Water Quality 12, no. 3 (1997): 245–48. http://dx.doi.org/10.1002/(sici)1098-2256(1997)12:3<245::aid-tox7>3.0.co;2-8.

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6

Stewart, Alex G., and Ewan Wilkinson. "Population Health Screening after Environmental Pollution." Geosciences 10, no. 12 (November 24, 2020): 477. http://dx.doi.org/10.3390/geosciences10120477.

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Following environmental pollution exposure, calls to screen the population for disease or disease markers are often made. Population screening is a cross-sectional review of a population to find latent cases or biomarkers of disease that indicate the possibility of disease development; it differs from environmental screening or an epidemiological survey. Recognized standard approaches have been developed over 60 years to ensure quality and effectiveness in complex programs. We surveyed the literature for papers on health screening following environmental exposures and checked them for reference to accepted criteria such as those of Wilson and Jungner. We applied these criteria to three situations covering source/hazard (arsenic contaminated land), pathway/exposure (radiation release), and receptor/disease (lead poisoning). We identified 36 relevant papers. Although across the papers the whole range of criteria were addressed, no paper or program utilized recognized criteria. Issues and gaps identified included limited strategic approaches, lack of treatment, environmental prevention being seen as the screening outcome instead of treatment of identified individuals, and programs which did not fit the World Health Organization screening description. Robust discussion in the literature is needed to consider the organization and role of health screening following environmental exposures.
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7

Haq, Arinil, Umar Fahmi Achmadi, and Anwar Mallongi. "Environmental Health Risk Assessment Due to Exposure to Mercury in Artisanal and Small-Scale Gold Mining Area of Lebak District." Global Journal of Health Science 10, no. 3 (February 12, 2018): 125. http://dx.doi.org/10.5539/gjhs.v10n3p125.

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In Indonesia it is estimated that there are around 250,000 artisanal and small-scale gold mining (ASGM) and generally use mercury for amalgamation process and then release it to the environment during gold refining process. This study aims to analyze mercury levels in the environment around ASGM in Lebaksitu Sub-District, Lebak District, Banten Province and identify hazardous exposure that may occur. The study design used was descriptive observational with Environmental Health Risk Assessment (EHRA) method. Environmental data taken include water and food samples. Social-demographic and dietary interviews were conducted. The study population was 72 residents of Lebaksitu Sub-District obtained through sample size formula and selected by simple random sampling. The study was conducted from April to May 2017. Exposure assessment is an important part of risk assessment. Exposure is a process that causes contact with environmental hazards such as risk agents, as a bridge connecting 'hazards' to 'risks'. Exposure analysis needs to consider all routes (inhalation, ingestion, absorption) and media (air, water, soil, food, drinking water) so that the total intake can be calculated. Exposure route analysis usually generate a critical pathway, the dominant exposure path. This pathway concerns which environmental media is the vehicle of risk agent and how it enters the body. Once a critical pathway is found, other possibility pathways contribution may be small and can be ignored. Mercury is a toxic pollutant that bioaccumulated and biomagnetic continuously through the food chain. The levels of mercury at the research sites on rice, fish, and vegetables have average of 0.027 mg/kg; 0.283 mg/kg; and 0.410 mg/kg. The calculation of risk assessment obtained value of risk quotient (RQ) of 3.79 (RQ>1). The results of this calculation of risk assessment showed that mercury content in samples of rice, fish, and vegetables originating from Lebaksitu Sub-District potentially cause a health risk for the community surrounding the gold mining area who consume it.
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8

Giovanoulis, Georgios, Thuy Bui, Fuchao Xu, Eleni Papadopoulou, Juan A. Padilla-Sanchez, Adrian Covaci, Line S. Haug, et al. "Multi-pathway human exposure assessment of phthalate esters and DINCH." Environment International 112 (March 2018): 115–26. http://dx.doi.org/10.1016/j.envint.2017.12.016.

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Zhang, Lianying, Xiaoyu Duan, Weijie Sun, and Hongwen Sun. "Perfluorooctane sulfonate acute exposure stimulates insulin secretion via GPR40 pathway." Science of The Total Environment 726 (July 2020): 138498. http://dx.doi.org/10.1016/j.scitotenv.2020.138498.

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10

Succop, P., R. Bornschein, K. Brown, and C. Y. Tseng. "An empirical comparison of lead exposure pathway models." Environmental Health Perspectives 106, suppl 6 (December 1998): 1577–83. http://dx.doi.org/10.1289/ehp.98106s61577.

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Ronoh, Patrick, Claire Furlong, Frank Kansiime, Richard Mugambe, and Damir Brdjanovic. "Are There Seasonal Variations in Faecal Contamination of Exposure Pathways? An Assessment in a Low–Income Settlement in Uganda." International Journal of Environmental Research and Public Health 17, no. 17 (September 1, 2020): 6355. http://dx.doi.org/10.3390/ijerph17176355.

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Sanitation infrastructure are not able to cope with the increasing population in low-income countries, which leaves populations exposed to faecal contamination from multiple pathways. This study evaluated public health risk (using SaniPath) in a low-income community during the dry season, to identify the dominant exposure pathways, and compare this data to existing data for the rainy season, questioning the assumption that risk of faecal contamination is higher in the rainy season. SaniPath was used to collect and assess exposure and environmental data, and to generate risk profiles for each pathway. In the dry season the highest exposure frequency was for bathing and street food, exposure frequency generally increased, and seasonal variation was found in five pathways. The highest hazards in the dry season were through contact with drains, soil, and street food. Seasonal variation was found in the contamination of open drains and street food, with higher levels of Escherichia coli (E. coli) in the dry season. Open drains were identified as the most dominant risk pathway in both seasons, but risk was higher in the dry season. This highlights the complex nature of seasonal variation of faecal risk, and questions the assumption that risk is higher in the rainy season.
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12

Svoboda, Laurie K., Kai Wang, Tamara R. Jones, Justin A. Colacino, Maureen A. Sartor, and Dana C. Dolinoy. "Sex-Specific Alterations in Cardiac DNA Methylation in Adult Mice by Perinatal Lead Exposure." International Journal of Environmental Research and Public Health 18, no. 2 (January 12, 2021): 577. http://dx.doi.org/10.3390/ijerph18020577.

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Environmental factors play an important role in the etiology of cardiovascular diseases. Cardiovascular diseases exhibit marked sexual dimorphism; however, the sex-specific effects of environmental exposures on cardiac health are incompletely understood. Perinatal and adult exposures to the metal lead (Pb) are linked to several adverse cardiovascular outcomes, but the sex-specific effects of this toxicant on the heart have received little attention. Perinatal environmental exposures can lead to disease through disruption of the normal epigenetic programming that occurs during early development. Using a mouse model of human-relevant perinatal environmental exposure, we investigated the effects of exposure to Pb during gestation and lactation on DNA methylation in the hearts of adult offspring mice (n = 6 per sex). Two weeks prior to mating, dams were assigned to control or Pb acetate (32 ppm) water, and exposure continued until offspring were weaned at three weeks of age. Enhanced reduced-representation bisulfite sequencing was used to measure DNA methylation in the hearts of offspring at five months of age. Although Pb exposure stopped at three weeks of age, we discovered hundreds of differentially methylated cytosines (DMCs) and regions (DMRs) in males and females at five months of age. DMCs/DMRs and their associated genes were sex-specific, with a small, but statistically significant subset overlapping between sexes. Pathway analysis revealed altered methylation of genes important for cardiac and other tissue development in males, and histone demethylation in females. Together, these data demonstrate that perinatal exposure to Pb induces sex-specific changes in cardiac DNA methylation that are present long after cessation of exposure, and highlight the importance of considering sex in environmental epigenetics and mechanistic toxicology studies.
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Teeguarden, Justin G., Yu-Mei Tan, Stephen W. Edwards, Jeremy A. Leonard, Kim A. Anderson, Richard A. Corley, Molly L. Kile, et al. "Completing the Link between Exposure Science and Toxicology for Improved Environmental Health Decision Making: The Aggregate Exposure Pathway Framework." Environmental Science & Technology 50, no. 9 (February 10, 2016): 4579–86. http://dx.doi.org/10.1021/acs.est.5b05311.

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14

Ioannidou, Despoina, Laure Malherbe, Maxime Beauchamp, Nicolas Saby, Roseline Bonnard, and Julien Caudeville. "Characterization of Environmental Health Inequalities Due to Polyaromatic Hydrocarbon Exposure in France." International Journal of Environmental Research and Public Health 15, no. 12 (November 28, 2018): 2680. http://dx.doi.org/10.3390/ijerph15122680.

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Reducing environmental health inequalities has become a major focus of public health efforts in France, as evidenced by the French action plans for health and the environment. To evaluate environmental inequalities, routine monitoring networks provide a valuable source of data on environmental contamination, which can be used in integrated assessments, to identify overexposed populations and prioritize actions. However, available databases generally do not meet sufficient spatial representativeness to characterize population exposure, as they are usually not assembled for this specific purpose. The aim of this study was to develop geoprocessing procedures and statistical methods to build spatial environmental variables (water, air, soil, and food pollutant concentrations) at a fine resolution, and provide appropriate input for the exposure modelling. Those methods were designed to combine in situ monitoring data with correlated auxiliary information (for example, atmospheric emissions, population, and altitude), in order to better represent the variability of the environmental compartment quality. The MODUL’ERS multimedia exposure model developed by INERIS (French Institute for industrial Environment and Risks) was then used to assess the transfer of substances from the environment to humans, through inhalation and ingestion pathway characterization. We applied the methodology to a carcinogenic Polycyclic Aromatic Hydrocarbon substance, benzo[a]pyrene(B[a]P), to map spatialized exposure indicators, at the national scale. The largest environmental contribution corresponded to the ingestion pathway. Data processing algorithms and calculation of exposure will be integrated into the French coordinated integrated environment and health platform PLAINE (PLteforme intégrée d’Analyse des INégalités Environnementales) which has been developed to map and analyze environmental health inequalities.
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Nabgha-e-Amen, Syed Ali Musstjab Akber Shah Eqani, Faiza Khuram, Ambreen Alamdar, Ayesha Tahir, Syed Tahir Abbas Shah, Arshan Nasir, et al. "Environmental exposure pathway analysis of trace elements and autism risk in Pakistani children population." Science of The Total Environment 712 (April 2020): 136471. http://dx.doi.org/10.1016/j.scitotenv.2019.136471.

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16

Núñez, Ana I., Anna Esteve-Codina, Jèssica Gómez-Garrido, Marco Brustolin, Sandra Talavera, Miguel Berdugo, Marc Dabad, Tyler Alioto, Albert Bensaid, and Núria Busquets. "Alteration in the Culex pipiens transcriptome reveals diverse mechanisms of the mosquito immune system implicated upon Rift Valley fever phlebovirus exposure." PLOS Neglected Tropical Diseases 14, no. 12 (December 10, 2020): e0008870. http://dx.doi.org/10.1371/journal.pntd.0008870.

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Rift Valley fever phlebovirus (RVFV) causes an emerging zoonotic disease and is mainly transmitted by Culex and Aedes mosquitoes. While Aedes aegypti-dengue virus (DENV) is the most studied model, less is known about the genes involved in infection-responses in other mosquito-arboviruses pairing. The main objective was to investigate the molecular responses of Cx. pipiens to RVFV exposure focusing mainly on genes implicated in innate immune responses. Mosquitoes were fed with blood spiked with RVFV. The fully-engorged females were pooled at 3 different time points: 2 hours post-exposure (hpe), 3- and 14-days post-exposure (dpe). Pools of mosquitoes fed with non-infected blood were also collected for comparisons. Total RNA from each mosquito pool was subjected to RNA-seq analysis and a de novo transcriptome was constructed. A total of 451 differentially expressed genes (DEG) were identified. Most of the transcriptomic alterations were found at an early infection stage after RVFV exposure. Forty-eight DEG related to immune infection-response were characterized. Most of them were related with the RNAi system, Toll and IMD pathways, ubiquitination pathway and apoptosis. Our findings provide for the first time a comprehensive view on Cx. pipiens-RVFV interactions at the molecular level. The early depletion of RNAi pathway genes at the onset of the RVFV infection would allow viral replication in mosquitoes. While genes from the Toll and IMD immune pathways were altered in response to RVFV none of the DEG were related to the JAK/STAT pathway. The fact that most of the DEG involved in the Ubiquitin-proteasome pathway (UPP) or apoptosis were found at an early stage of infection would suggest that apoptosis plays a regulatory role in infected Cx. pipiens midguts. This study provides a number of target genes that could be used to identify new molecular targets for vector control.
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Noonan, Curtis W., Kathrene Conway, Erin L. Landguth, Tracy McNew, Laura Linker, Jean Pfau, Brad Black, Jaime Szeinuk, and Raja Flores. "Multiple pathway asbestos exposure assessment for a Superfund community." Journal of Exposure Science & Environmental Epidemiology 25, no. 1 (April 23, 2014): 18–25. http://dx.doi.org/10.1038/jes.2014.25.

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18

Anderson, Barbara A., Steve M. Dearwent, James T. Durant, Jill J. Dyken, Jennifer A. Freed, Susan McAfee Moore, and John S. Wheeler. "Exposure pathway evaluations for sites that processed asbestos-contaminated vermiculite." International Journal of Hygiene and Environmental Health 208, no. 1-2 (April 2005): 55–65. http://dx.doi.org/10.1016/j.ijheh.2005.01.008.

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19

Barnhill, Lisa M., Sataree Khuansuwan, Daniel Juarez, Hiromi Murata, Jesus A. Araujo, and Jeff M. Bronstein. "Diesel Exhaust Extract Exposure Induces Neuronal Toxicity by Disrupting Autophagy." Toxicological Sciences 176, no. 1 (April 16, 2020): 193–202. http://dx.doi.org/10.1093/toxsci/kfaa055.

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Abstract The vast majority of neurodegenerative disease cannot be attributed to genetic causes alone and as a result, there is significant interest in identifying environmental modifiers of disease risk. Epidemiological studies have supported an association between long-term exposure to air pollutants and disease risk. Here, we investigate the mechanisms by which diesel exhaust, a major component of air pollution, induces neurotoxicity. Using a zebrafish model, we found that exposure to diesel exhaust particulate extract caused behavioral deficits and a significant decrease in neuron number. The neurotoxicity was due, at least in part, to reduced autophagic flux, which is a major pathway implicated in neurodegeneration. This neuron loss occurred alongside an increase in aggregation-prone neuronal protein. Additionally, the neurotoxicity induced by diesel exhaust particulate extract in zebrafish was mitigated by co-treatment with the autophagy-inducing drug nilotinib. This study links environmental exposure to altered proteostasis in an in vivo model system. These results shed light on why long-term exposure to traffic-related air pollution increases neurodegenerative disease risk and open up new avenues for exploring therapies to mitigate environmental exposures and promote neuroprotection.
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Kendler, K. S., and C. O. Gardner. "A longitudinal etiologic model for symptoms of anxiety and depression in women." Psychological Medicine 41, no. 10 (April 11, 2011): 2035–45. http://dx.doi.org/10.1017/s0033291711000225.

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BackgroundDesigned as state measures to monitor treatment response, symptoms of anxiety and depression (SxAnxDep) also have trait-like characteristics. No comprehensive etiologic model for SxAnxDep has illuminated the inter-relationship between their state- and trait-like characteristics, while including key predictor variables.MethodIn a prospective three-wave study of 2395 female twins from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders (VATSPSUD), we examined, using structural equation modeling, how genes, childhood and past-year environmental stressors, personality and episodes of major depression (MD) and generalized anxiety disorder (GAD) influence SxAnxDep.ResultsThe best-fit model, which explained 68–74% of the variance in SxAnxDep, revealed two etiologic pathways. Stable levels of SxAnxDep resulted largely from neuroticism, which in turn was influenced by genetic and early environment risk factors. Occasion-specific influences resulted from stressful events mediated through episodes of MD or GAD. These two pathways, which had approximately equal influences on levels of SxAnxDep, were substantially correlated because the genetic, early environmental and personality factors that impacted on stable symptom levels also predisposed to event exposure and disorder onset. No significant interaction was seen between the two pathways.ConclusionsSxAnxDep in women in the general population arise from two inter-related causal pathways. The first, the ‘trait-like’ pathway, reflects genetic and early environmental risk factors, and is mediated largely through personality. The second pathway is mediated through episodes of MD and GAD, and is the result of both recent environmental adversities and trait-like factors that influence event exposure and the probability of disorder onset.
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Tokumura, Masahiro, Makiko Seo, Qi Wang, Yuichi Miyake, Takashi Amagai, and Masakazu Makino. "Dermal exposure to plasticizers in nail polishes: An alternative major exposure pathway of phosphorus-based compounds." Chemosphere 226 (July 2019): 316–20. http://dx.doi.org/10.1016/j.chemosphere.2019.03.108.

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22

Wood, Chris M., Natasha M. Franklin, and Som Niyogi. "The Protective Role of Dietary Calcium Against Cadmium Uptake and Toxicity in Freshwater Fish: an Important Role for the Stomach." Environmental Chemistry 3, no. 6 (2006): 389. http://dx.doi.org/10.1071/en06056.

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Environmental Context. Contamination of freshwater ecosystems by cadmium is of increasing concern with accumulation and toxicity in aquatic animals occurring through both waterborne and dietary routes. Increases in water calcium (‘hardness’) levels protect against waterborne uptake. Physiological research on freshwater fish has demonstrated that this occurs because cadmium moves through the calcium uptake pathway at the gills. Surprisingly, elevated dietary calcium also protects against waterborne exposure by down-regulating the calcium uptake pathway at the gills, and against dietary exposure by reducing cadmium uptake through the gastrointestinal tract. In both cases, the stomach is the critical site of action. Abstract. Waterborne cadmium causes toxicity in freshwater fish by inducing hypocalcaemia. Research on the rainbow trout (Oncorhynchus mykiss), a sensitive model species, has demonstrated that this occurs because Cd2+ ions compete with waterborne Ca2+ ions for the active branchial uptake pathway which normally ensures internal homeostasis of calcium levels. Therefore, increases in waterborne calcium concentrations (‘hardness’) protect against waterborne cadmium uptake and toxicity in both acute and chronic exposures. Increases in dietary calcium concentration also protect against waterborne exposure, because elevated gastrointestinal calcium uptake down-regulates the Ca2+ uptake pathway at the gills, thereby simultaneously reducing Cd2+ entry. Furthermore, dietary calcium also protects against dietborne cadmium exposure, although the physiological mechanisms appear to differ from those at the gills. Surprisingly, the principal site of this inhibitory action of dietary calcium on gastrointestinal cadmium uptake appears to be the stomach, which is also the major site of gastrointestinal calcium uptake, rather than the intestine as in mammals. These results underline the importance of considering not only water chemistry but also dietary chemistry in the environmental regulation of cadmium, and suggest that fish in the wild under chronic cadmium stress would benefit by switching to a more calcium-rich diet. While diet switching has been seen in the wild in fish under metal stress, its etiology remains unknown; to date, laboratory experiments have not been able to show that voluntary diet-switching of an adaptive nature actually occurs.
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Uyak, Vedat. "Multi-pathway risk assessment of trihalomethanes exposure in Istanbul drinking water supplies." Environment International 32, no. 1 (January 2006): 12–21. http://dx.doi.org/10.1016/j.envint.2005.03.005.

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Malakar, Arindam, Sushil R. Kanel, Chittaranjan Ray, Daniel D. Snow, and Mallikarjuna N. Nadagouda. "Nanomaterials in the environment, human exposure pathway, and health effects: A review." Science of The Total Environment 759 (March 2021): 143470. http://dx.doi.org/10.1016/j.scitotenv.2020.143470.

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Dickinson, JL, DI Perera, AF van der Mei, A.-L. Ponsonby, AM Polanowski, RJ Thomson, BV Taylor, JD McKay, J. Stankovich, and T. Dwyer. "Past environmental sun exposure and risk of multiple sclerosis: a role for the Cdx-2 Vitamin D receptor variant in this interaction." Multiple Sclerosis Journal 15, no. 5 (April 21, 2009): 563–70. http://dx.doi.org/10.1177/1352458509102459.

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Multiple studies have provided evidence for an association between reduced sun exposure and increased risk of multiple sclerosis (MS), an association likely to be mediated, at least in part, by the vitamin D hormonal pathway. Herein, we examine whether the vitamin D receptor ( VDR), an integral component of this pathway, influences MS risk in a population-based sample where winter sun exposure in early childhood has been found to be an important determinant of MS risk. Three polymorphisms within the VDR gene were genotyped in 136 MS cases and 235 controls, and associations with MS and past sun exposure were examined by logistic regression. No significant univariate associations between the polymorphisms, rs11574010 ( Cdx-2A > G), rs10735810 ( Fok1T > C), or rs731236 ( Taq1C > T) and MS risk were observed. However, a significant interaction was observed between winter sun exposure during childhood, genotype at rs11574010, and MS risk ( P = 0.012), with the ‘G’ allele conferring an increased risk of MS in the low sun exposure group (≤2 h/day). No significant interactions were observed for either rs10735810 or rs731236, after stratification by sun exposure. These data provide support for the involvement of the VDR gene in determining MS risk, an interaction likely to be dependent on past sun exposure.
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Cheng, Jie, Na Li, Zhe Cheng, Renping Hua, Jingwei Cai, Wenhui Si, and Fashui Hong. "Splenocyte apoptotic pathway in mice following oral exposure to cerium trichloride." Chemosphere 83, no. 4 (April 2011): 612–17. http://dx.doi.org/10.1016/j.chemosphere.2010.12.013.

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Beaubien, Gale B., Connor I. Olson, Andrew C. Todd, and Ryan R. Otter. "The Spider Exposure Pathway and the Potential Risk to Arachnivorous Birds." Environmental Toxicology and Chemistry 39, no. 11 (September 22, 2020): 2314–24. http://dx.doi.org/10.1002/etc.4848.

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Svoboda, Laurie K., Kai Wang, Raymond G. Cavalcante, Kari Neier, Justin A. Colacino, Maureen A. Sartor, and Dana C. Dolinoy. "Sex-Specific Programming of Cardiac DNA Methylation by Developmental Phthalate Exposure." Epigenetics Insights 13 (January 2020): 251686572093997. http://dx.doi.org/10.1177/2516865720939971.

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Phthalate plasticizers are ubiquitous chemicals linked to several cardiovascular diseases in animal models and humans. Despite this, the mechanisms by which phthalate exposures cause adverse cardiac health outcomes are unclear. In particular, whether phthalate exposures during pregnancy interfere with normal developmental programming of the cardiovascular system, and the resulting implications this may have for long-term disease risk, are unknown. Recent studies suggest that the effects of phthalates on metabolic and neurobehavioral outcomes are sex-specific. However, the influence of sex on cardiac susceptibility to phthalate exposures has not been investigated. One mechanism by which developmental exposures may influence long-term health is through altered programming of DNA methylation. In this work, we utilized an established mouse model of human-relevant perinatal exposure and enhanced reduced representation bisulfite sequencing to investigate the long-term effects of diethylhexyl phthalate (DEHP) exposure on DNA methylation in the hearts of adult male and female offspring at 5 months of age (n = 5-7 mice per sex and exposure). Perinatal DEHP exposure led to hundreds of sex-specific, differentially methylated cytosines (DMCs) and differentially methylated regions (DMRs) in the heart. Pathway analysis of DMCs revealed enrichment for several pathways in females, including insulin signaling, regulation of histone methylation, and tyrosine phosphatase activity. In males, DMCs were enriched for glucose transport, energy generation, and developmental programs. Notably, many sex-specific genes differentially methylated with DEHP exposure in our mouse model were also differentially methylated in published data of heart tissues collected from human heart failure patients. Together, these data highlight the potential role for DNA methylation in DEHP-induced cardiac effects and emphasize the importance of sex as a biological variable in environmental health studies.
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Amstadter, Ananda B., Steven H. Aggen, Gun Peggy Knudsen, Ted Reichborn-Kjennerud, and Kenneth S. Kendler. "A Population-Based Study of Familial and Individual-Specific Environmental Contributions to Traumatic Event Exposure and Posttraumatic Stress Disorder Symptoms in a Norwegian Twin Sample." Twin Research and Human Genetics 15, no. 5 (July 3, 2012): 656–62. http://dx.doi.org/10.1017/thg.2012.43.

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Objective: Posttraumatic stress disorder (PTSD) is one of the only disorders in the Diagnostic and Statistical Manual of Mental Disorders that requires an environmental exposure. The relationship between liability factors for trauma exposure and those for PTSD symptoms following exposure are unclear. Methods: Exposure to a trauma and resulting PTSD symptoms were assessed in a sample of 2,794 members of the Norwegian Institute of Public Health Twin Panel. Results: In the full sample, 737 twins experienced a trauma. A modified causal, contingent, common pathway model was used to examine trauma exposure and liability for PTSD. Genetic and common environmental factors could not be distinguished, so a model that included only familial and individual specific components was fit. The best-fitting model suggested that familial factors played an important role in liability for trauma exposure and for resulting PTSD symptoms, and that there was a modest transmission between trauma exposure and subsequent PTSD symptoms. Conclusions: One third of the variance in liability of PTSD symptoms is due to familial factors, and of this, approximately one fifth overlaps with the familial liability for trauma exposure while the other four fifths of the variance is specific to the risk of PTSD symptoms following exposure. The hypothesis that PTSD is etiologically similar to exposures to a traumatic event is not supported, suggesting that the factors that confer risk for trauma do not overlap completely with those that confer risk for PTSD.
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30

Currier, Nicolas, Sandra E. Solomon, Elizabeth G. Demicco, Donny L. F. Chang, Marganit Farago, Haoqiang Ying, Isabel Dominguez, et al. "Oncogenic Signaling Pathways Activated in DMBA-Induced Mouse Mammary Tumors." Toxicologic Pathology 33, no. 6 (October 2005): 726–37. http://dx.doi.org/10.1080/01926230500352226.

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Only about 5% of human breast cancers can be attributed to inheritance of breast cancer susceptibility genes, while the balance are considered to be sporadic in origin. Breast cancer incidence varies with diet and other environmental influences, including carcinogen exposure. However, the effects of environmental carcinogens on cell growth control pathways are poorly understood. Here we have examined oncogenic signaling pathways that are activated in mammary tumors in mice treated with the prototypical polycyclic aromatic hydrocarbon (PAH) 7,12-dimethylbenz[ a]anthracene (DMBA). In female FVB mice given 6 doses of 1 mg of DMBA by weekly gavage beginning at 5 weeks of age, all of the mice developed tumors by 34 weeks of age (median 20 weeks after beginning DMBA); 75% of the mice had mammary tumors. DMBA-induced mammary tumors exhibited elevated expression of the aryl hydrocarbon receptor (AhR), c- myc, cyclin D1, and hyperphosphorylated retinoblastoma (Rb) protein. Because of this, the activation of upstream regulatory pathways was assessed, and elements of the Wnt signaling pathway, the NF-κB pathway, and the prolyl isomerase Pin-1 were found to be frequently up-regulated in the tumors when compared to normal mammary gland controls. These data suggest that environmental carcinogens can produce long-lasting alterations in growth and anti-apoptotic pathways, leading to mammary tumorigenesis.
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Anderson, Olivia S., Jung H. Kim, Karen E. Peterson, Brisa N. Sanchez, Karilyn E. Sant, Maureen A. Sartor, Caren Weinhouse, and Dana C. Dolinoy. "Novel Epigenetic Biomarkers Mediating Bisphenol A Exposure and Metabolic Phenotypes in Female Mice." Endocrinology 158, no. 1 (November 8, 2016): 31–40. http://dx.doi.org/10.1210/en.2016-1441.

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Abstract There is compelling evidence that epigenetic modifications link developmental environmental insults to adult disease susceptibility. Animal studies have associated perinatal bisphenol A (BPA) exposure to altered DNA methylation, but these studies are often limited to candidate gene and global non–loci-specific approaches. By using an epigenome-wide discovery platform, we elucidated epigenetic alterations in liver tissue from adult mice offspring (10 months) following perinatal BPA exposure at human physiologically relevant doses (50-ng, 50-μg, and 50-mg BPA/kg diet). Biological pathway analysis identified an enrichment of significant differentially methylated regions in metabolic pathways among females. Furthermore, through the use of top enriched biological pathways, 4 candidate genes were chosen to assess DNA methylation as a mediating factor linking the association of perinatal BPA exposure to metabolic phenotypes previously observed in female offspring. DNA methylation status at Janus kinase-2 (Jak-2), retinoid X receptor (Rxr), regulatory factor x-associated protein (Rfxap), and transmembrane protein 238 (Tmem238) was used within a mediational regression analysis. DNA methylation in all four of the candidate genes was identified as a mediator in the mechanistic pathway of developmental BPA exposure and female-specific energy expenditure, body weight, and body fat phenotypes. Data generated from this study are crucial for deciphering the mechanistic role of epigenetics in the pathogenesis of chronic disease and the development of epigenetic-based prevention and therapeutic strategies for complex human disease.
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Ernstoff, Alexi, Monia Niero, Jane Muncke, Xenia Trier, Ralph K. Rosenbaum, Michael Hauschild, and Peter Fantke. "Challenges of including human exposure to chemicals in food packaging as a new exposure pathway in life cycle impact assessment." International Journal of Life Cycle Assessment 24, no. 3 (December 12, 2018): 543–52. http://dx.doi.org/10.1007/s11367-018-1569-y.

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Nawrot, Tim S., Nelly D. Saenen, Julie Schenk, Bram G. Janssen, Valeria Motta, Letizia Tarantini, Bianca Cox, et al. "Placental circadian pathway methylation and in utero exposure to fine particle air pollution." Environment International 114 (May 2018): 231–41. http://dx.doi.org/10.1016/j.envint.2018.02.034.

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34

Padmanabhan, Vasantha, Rodolfo C. Cardoso, and Muraly Puttabyatappa. "Developmental Programming, a Pathway to Disease." Endocrinology 157, no. 4 (February 9, 2016): 1328–40. http://dx.doi.org/10.1210/en.2016-1003.

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Abstract Accumulating evidence suggests that insults occurring during the perinatal period alter the developmental trajectory of the fetus/offspring leading to long-term detrimental outcomes that often culminate in adult pathologies. These perinatal insults include maternal/fetal disease states, nutritional deficits/excess, stress, lifestyle choices, exposure to environmental chemicals, and medical interventions. In addition to reviewing the various insults that contribute to developmental programming and the benefits of animal models in addressing underlying mechanisms, this review focuses on the commonalities in disease outcomes stemming from various insults, the convergence of mechanistic pathways via which various insults can lead to common outcomes, and identifies the knowledge gaps in the field and future directions.
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35

Jiang, Shu-Lun, Di-An Fang, and Dong-Po Xu. "Transcriptome changes of Takifugu obscurus liver after acute exposure to phenanthrene." Physiological Genomics 53, no. 3 (March 1, 2021): 116–24. http://dx.doi.org/10.1152/physiolgenomics.00100.2020.

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Phenanthrene (Phe) is a model compound in polycyclic aromatic hydrocarbon (PAH) research. Reportedly, Phe treatment induced oxidative stress and histological disorders to Takifugu obscurus liver. In this study, to further explore the molecular responses of T. obscurus liver to Phe exposure, transcriptome sequencing was applied to compare mRNA transcription profiles between Phe treatment and the control. Compared with the control, 1,581 and 1,428 genes were significantly upregulated and downregulated in Phe treatment, respectively. Further analysis revealed that Phe treatment mainly upregulated genes in Ras-MAPK and PI3K-akt signaling pathways, which represented insulin resistance and further activated the FOXO signaling pathway. The triacylglycerol biosynthesis was promoted but the gluconeogenesis process was inhibited in response to Phe treatment, demonstrating that Phe exposure disturbed the sugar and lipid metabolism. Moreover, Phe treatment upregulated the Apelin-APJ and ErbB signaling pathways, promoting angiogenesis in T. obscurus liver. Insulin resistance, promoted triacylglycerol biosynthesis, and angiogenesis might explain the molecular mechanisms underlying carcinogenic toxicity of Phe. Overall, this study provides new insights to understand the environmental risk of Phe to fishes.
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36

Spauwen, Janneke, and Jim Van Os. "The psychosis proneness: psychosis persistence model as an explanation for the association between urbanicity and psychosis." Epidemiology and Psychiatric Sciences 15, no. 4 (December 2006): 252–57. http://dx.doi.org/10.1017/s1121189x00002128.

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AbstractGiven the relatively high attributable risks associated with urbanicity it is crucially important to learn more on how this exposure impacts on population risk for schizophrenia. Further elucidation of the environmental influences that currently go under the name of “urbanicity” therefore is a crucial step in unravelling the etiology of schizophrenia. In order to make the step from association to cause, a plausible mechanism detailing the pathway from impact of exposure to onset of psychotic symptoms is needed. This paper outlines possible avenues and clues to the identification of possible mechanisms and pathways. The focus is on mechanisms of gene-environment interaction in the context of both functional genetic polymorphisms and epigenetic variation.
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Feckler, Alexander, Willem Goedkoop, Jochen P. Zubrod, Ralf Schulz, and Mirco Bundschuh. "Exposure pathway-dependent effects of the fungicide epoxiconazole on a decomposer-detritivore system." Science of The Total Environment 571 (November 2016): 992–1000. http://dx.doi.org/10.1016/j.scitotenv.2016.07.088.

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38

Crush, Eloise, Louise Arseneault, Andrea Danese, Sara R. Jaffee, and Helen L. Fisher. "Using discordant twin methods to investigate an environmentally mediated pathway between social support and the reduced likelihood of adolescent psychotic experiences." Psychological Medicine 50, no. 11 (August 15, 2019): 1898–905. http://dx.doi.org/10.1017/s0033291719001983.

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AbstractBackgroundSocial support has been shown to be associated with a reduced likelihood of developing psychotic experiences in the general population and even amongst those at high risk due to exposure to multiple forms of victimisation (poly-victimised). However, it is unclear whether this association is merely due to the confounding effects of shared environmental and genetic influences, or reverse causality. Therefore, we investigated whether social support has a unique environmentally mediated effect on adolescent psychotic experiences after accounting for familial factors, including genetic factors, and also prior psychopathology.MethodsParticipants were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally-representative cohort of 2232 UK-born twins. Adolescents were interviewed at age 18 about psychotic experiences and victimisation exposure since age 12, and their perceptions of social support. Prior childhood mental health problems and psychotic symptoms were assessed at age 12. The discordant twin method was used to disentangle the relative family-wide and unique-environmental effects of social support on psychotic experiences in the general population and among poly-victimised adolescents.ResultsPerceived social support, particularly from friends, was found to have a unique environmentally mediated buffering effect on adolescent psychotic experiences in the whole sample and in the high-risk poly-victimised group.ConclusionsThe protective effects of social support on adolescent psychotic experiences cannot be accounted for by shared environmental or genetic factors, nor by earlier psychopathology. Our findings suggest that early intervention programmes focused on increasing perceptions of social support have the potential to prevent the emergence of psychotic experiences amongst adolescents.
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39

Ebenso, I. E., and A. D. Ologhobo. "Evaluation of environmental lead exposure in snails from four contaminated sites at abandoned battery factory in Niger Delta, Nigeria." Nigerian Journal of Animal Production 37, no. 2 (January 3, 2021): 258–63. http://dx.doi.org/10.51791/njap.v37i2.1361.

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The evaluation of environmental lead exposure in snails from four contaminated sites of entrance, storage, dried effluent and waste dump respectively, at abandoned battery factory (Niger Delta, Nigeria) were investigated Results indicated significant (P<0.05) depressed weights of foot, shell, and offal at elevated lead contamination. The exposure of Achatina achatina snail to lead pollution indicates a pollution warning signal. Contaminated snails are critical pathway for transport of lead along the food chain.
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40

Graziano, J. H. "Validity of lead exposure markers in diagnosis and surveillance." Clinical Chemistry 40, no. 7 (July 1, 1994): 1387–90. http://dx.doi.org/10.1093/clinchem/40.7.1387.

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Abstract Extensive research has been devoted to the development of biomarkers of environmental and occupational exposure to lead (Pb). This body of work can serve as a paradigm for biomarker development for other chemical exposures. Early efforts focused on indirect measurements of exposure by analyzing precursors and enzymes of a biosynthetic pathway (heme) in blood and urine. However, the direct measurement of Pb in blood has become increasingly simple and reliable and is now widely accepted for pediatric surveillance programs, in part because of known associations of Pb with adverse health outcomes. Other markers of exposure include measurements of Pb in important compartments: bone Pb, tooth Pb, and chelatable Pb. In addition, the technique of stable isotope dilution is available, since Pb exists in numerous nonradioactive isotopic forms. The strengths and weaknesses of all Pb biomarkers for confirming a diagnosis or for epidemiologic research vary widely depending upon the hypothesis under investigation.
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41

Jones-Otazo, Heather A., John P. Clarke, Miriam L. Diamond, Josephine A. Archbold, Glenn Ferguson, Tom Harner, G. Mark Richardson, John Jake Ryan, and Bryony Wilford. "Is House Dust the Missing Exposure Pathway for PBDEs? An Analysis of the Urban Fate and Human Exposure to PBDEs." Environmental Science & Technology 39, no. 14 (July 2005): 5121–30. http://dx.doi.org/10.1021/es048267b.

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42

Allibone, Rachel, Shane J. Cronin, Douglas T. Charley, Vince E. Neall, Robert B. Stewart, and Clive Oppenheimer. "Dental fluorosis linked to degassing of Ambrym volcano, Vanuatu: a novel exposure pathway." Environmental Geochemistry and Health 34, no. 2 (August 12, 2010): 155–70. http://dx.doi.org/10.1007/s10653-010-9338-2.

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43

Cossec, Benoît, Frédéric Cosnier, Manuella Burgart, Hervé Nunge, and Stéphane Grossmann. "Glutathione pathway in ethylbenzene metabolism: Novel biomarkers of exposure in the rat." Chemosphere 81, no. 10 (November 2010): 1334–41. http://dx.doi.org/10.1016/j.chemosphere.2010.08.025.

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44

Wang, Shengchen, Qiaojian Zhang, Shufang Zheng, Menghao Chen, Fuqing Zhao, and Shiwen Xu. "Atrazine exposure triggers common carp neutrophil apoptosis via the CYP450s/ROS pathway." Fish & Shellfish Immunology 84 (January 2019): 551–57. http://dx.doi.org/10.1016/j.fsi.2018.10.029.

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45

Sullivan, M. J., P. A. McCaw, R. L. Holmes, C. H. Sewall, and S. D. Surgenor. "Multiple exposure pathway risk assessment for dioxin at a bleached pulp mill." Chemosphere 20, no. 10-12 (January 1990): 1771–78. http://dx.doi.org/10.1016/0045-6535(90)90341-p.

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46

Zheng, Shufang, Xi Jin, Menghao Chen, Qunxiang Shi, Hongfu Zhang, and Shiwen Xu. "Hydrogen sulfide exposure induces jejunum injury via CYP450s/ROS pathway in broilers." Chemosphere 214 (January 2019): 25–34. http://dx.doi.org/10.1016/j.chemosphere.2018.09.002.

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47

Feduraev, Pavel, Liubov Skrypnik, Anastasiia Riabova, Artem Pungin, Elina Tokupova, Pavel Maslennikov, and Galina Chupakhina. "Phenylalanine and Tyrosine as Exogenous Precursors of Wheat (Triticum aestivum L.) Secondary Metabolism through PAL-Associated Pathways." Plants 9, no. 4 (April 9, 2020): 476. http://dx.doi.org/10.3390/plants9040476.

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Reacting to environmental exposure, most higher plants activate secondary metabolic pathways, such as the metabolism of phenylpropanoids. This pathway results in the formation of lignin, one of the most important polymers of the plant cell, as well as a wide range of phenolic secondary metabolites. Aromatic amino acids, such as phenylalanine and tyrosine, largely stimulate this process, determining two ways of lignification in plant tissues, varying in their efficiency. The current study analyzed the effect of phenylalanine and tyrosine, involved in plant metabolism through the phenylalanine ammonia-lyase (PAL) pathway, on the synthesis and accumulation of phenolic compounds, as well as lignin by means of the expression of a number of genes responsible for its biosynthesis, based on the example of common wheat (Triticum aestivum L.).
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48

Ishii, Seiji, Toru Sasaki, Shahid Mohammad, Hye Hwang, Edwin Tomy, Fahad Somaa, Nobuyuki Ishibashi, et al. "Primary cilia safeguard cortical neurons in neonatal mouse forebrain from environmental stress-induced dendritic degeneration." Proceedings of the National Academy of Sciences 118, no. 1 (December 21, 2020): e2012482118. http://dx.doi.org/10.1073/pnas.2012482118.

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The developing brain is under the risk of exposure to a multitude of environmental stressors. While perinatal exposure to excessive levels of environmental stress is responsible for a wide spectrum of neurological and psychiatric conditions, the developing brain is equipped with intrinsic cell protection, the mechanisms of which remain unknown. Here we show, using neonatal mouse as a model system, that primary cilia, hair-like protrusions from the neuronal cell body, play an essential role in protecting immature neurons from the negative impacts of exposure to environmental stress. More specifically, we found that primary cilia prevent the degeneration of dendritic arbors upon exposure to alcohol and ketamine, two major cell stressors, by activating cilia-localized insulin-like growth factor 1 receptor and downstream Akt signaling. We also found that activation of this pathway inhibits Caspase-3 activation and caspase-mediated cleavage/fragmentation of cytoskeletal proteins in stress-exposed neurons. These results indicate that primary cilia play an integral role in mitigating adverse impacts of environmental stressors such as drugs on perinatal brain development.
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49

Adamec, Robert. "Modelling Anxiety Disorders Following Chemical Exposures." Toxicology and Industrial Health 10, no. 4-5 (July 1994): 391–420. http://dx.doi.org/10.1177/074823379401000513.

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The effects of kindling and inverse benzodiazepine receptor agonist -carbolines on animal models of anxiety are briefly reviewed in relation to affective disorder associated with chemical exposure. Recent experimental results are described. In the present study, cats were given the inverse benzodiazepine receptor agonist, FG-7142, a powerful anxiogenic compound in humans and animals. Neural transmission in pathways involved in defensive behavior in the cat was monitored using evoked potential techniques. Change in these pathways was related to behavioral changes induced by the drug. It was found that a single dose offG-7142 lastingly increased defensive response to rodents for at least 40 days after drug administration. Behavioral change was specific to defensive response, since approach-attack behavior remained unchanged, replicating previous studies. The benzodiazepine receptor antagonist, Flumazenil, reversed the increase in defensiveness in a drug-dependent manner, replicating previous findings. Increased defensiveness was paralleled by a delayed onset potentiation of neural transmission between the amygdala and the medial hypothalamus of the left hemisphere. Potentiation in the left hemisphere was transient, decaying between 6 and 12 days after the drug. There was a longer lasting potentiation (LTP) of activity evoked in the left and right amygdalo-periacqueductal gray pathways and in the right amygdalo-medial hypothalamic pathway. Potentiation in these pathways appeared at the time of behavioral change. Potentiation of the right amygdalo-periacqueductal gray and right amygdalo-medial hypothalamic pathways persisted until the end of the experiment. In contrast, potentiation of the left amygdalo-periacqueductal gray pathway faded by 40 days after the drug. Flumazenil decreased potentiation only in the right amygdalo-periacqueductal gray pathway. These data strongly suggest that lasting affective change is mediated by lasting changes in particular efferents of the amygdala of the right hemisphere. Behavioral and physiological effects offG-7142 were blocked by the N-methyl-D-Aspartate (NMDA) receptor blocker, AP7. The data suggest that failure of neural inhibition induced by FG-7142 engages NMDA receptor processes to produce lasting potentiation of transmission in neural circuits that mediate defensive response with behavioral consequences. Since FG-7142 interferes with GABA mediated neural inhibition and is proconvulsant, its action might mimic the action of other environmental chemicals with similar properties, such as chlorinated hydrocarbon insecticides. The relationship of the present data to the literature on the neural and behavioral effects of insecticide exposure is discussed. The significance of these findings for multiple chemical sensitivity disorder is also briefly discussed.
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Pagliari, Bruna Garcia, Maria De Fátima Ramos Moreira, Camille Ferreira Mannarino, and Gideon Borges dos Santos. "Risk of exposure to metals in soil contaminated by steel industry waste for a population in Volta Redonda, RJ." Ambiente e Agua - An Interdisciplinary Journal of Applied Science 16, no. 4 (August 9, 2021): 1. http://dx.doi.org/10.4136/ambi-agua.2696.

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The aim of this study was to identify the risk of population’s exposure, by different exposure routes, to Zn, Ni, Cu, Cr, and Pb in the soil of a condominium. Six sampling points in three campaigns provided thirty-six soil samples, collected at two depths, one superficial, 0.20 m, and the other underground, between 2.00 and 3.00 m. The results show that the levels of metals in the condominium's soil are generally high. Children cannot withstand the same doses as adults since they are more susceptible and risk greater damage to health. The non-carcinogenic risk based on the hazard quotient (HQ) and the health index (HI) values for each exposure pathway and for each metal were observed to be less than (<) 1. The results showed an immediate carcinogenic risk by chromium ingestion for children. Nevertheless the combined effect for each exposure pathway (TCRI) for adults is close to becoming unacceptable after exposure to Cr by ingestion. The results suggest that contamination by metals is more likely to occur among children than adults at similar exposure levels. Thus, the condominium built on an area contaminated by steel industry waste raises concern, requiring the continuous monitoring of its population.
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