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Abstract

Background: Cancer stem cells (CSCs) drive tumor initiation, progression and metastasis. Microenvironment is critical to the fate of CSCs. We have found that a normal stem cell (NSC) line from human prostate (WPE-stem) is recruited into CSC-like cells by nearby, but noncontiguous arsenic-transformed isogenic malignant epithelial cells (MECs).

Objective: It is unknown if this recruitment of NSCs into CSCs by non-contact co-culture is specific to arsenic-transformed MECs. Thus, here, we tested the effects of neighboring noncontiguous cadmium-transformed MECs (Cd-MECs) and N-methyl-N-nitrosourea-transformed MECs (MNU-MECs) co-culture on NSCs.

Results: After two weeks of non-contact Cd-MEC co-culture, NSCs showed elevated metalloproteinase-9 (MMP-9) and MMP-2 secretion, increased invasiveness, increased colony formation, decreased PTEN expression and formation of aggressive, highly branched ductal-like structures from single cells in Matrigel, all characteristics typical of cancer cells. These oncogenic characteristics did not occur if NSCs were co-cultured with MNU-MECs. The NSCs co-cultured with Cd-MECs retained self-renewal capacity as evidenced by multiple passages (>3) of structures formed in Matrigel. Cd-MEC co-cultured NSCs also showed molecular (increased VIMENTIN, SNAIL1 and TWIST1 expression; decreased E-CADHERIN expression) and morphologic evidence of epithelial-to-mesenchymal transition typical for conversion to CSCs. Dysregulated expression of SC-renewal genes, including ABCG2, OCT-4 and WNT-3, also occurred in NSCs during oncogenic transformation induced by non-contact co-culture with Cd-MECs.

Conclusions: These data indicate that Cd-MECs can recruit nearby NSCs into a CSC-like phenotype, but MNU-MECs do not. Thus, the recruitment of NSCs into CSCs by nearby MECs is dependent on the carcinogen originally used to malignantly transform the MECs.

Citation: Xu Y, Tokar EJ, Person RJ, Orihuela RG, Ngalame NO, Waalkes MP. Environ Health Perspect (): .doi:10.1289/ehp.1306714

Received: February 26, 2013; Accepted: May 16, 2013; Published: May 17, 2013

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¹Department of Hygiene, Epidemiology and Medical Statistics, Medical School, University of Athens, Athens, Greece; ²Department of Epidemiology Lazio Region, Rome, Italy; ³Air Pollution Epidemiology Section, Office of Environmental Health Hazard Assessment, CAL EPA, Oakland, California U.S.A; ⁴Centre for Research in Environmental Epidemiology (CREAL), Barcelona Biomedical Research Park, Barcelona, Spain; ⁵Environmental Health Department, French Institute for Public Health Surveillance (InVS), Saint-Maurice, France; ⁶National School of Public Health, Carlos III Health Institute, Madrid, Spain; ⁷Institute of Environmental Assessment and Water Research (IDAEA-CSIC), Barcelona, Spain; ⁸Environmental Department, Municipality of Thessaloniki, Thessaloniki, Greece; ⁹Epidemiology Observatory, Department of Public Ηealth, Local Health Authority, Bologna, Italy; ¹⁰Epidemiology Unit, Local Health Authority, Milan, Italy; ¹¹Department of Epidemiology and Environmental Health, Regional Environmental Protection Agency, Piedmont, Italy; ¹²Regional Centre for Environment and Health, Regional Agency for Environmental Prevention of Emilia-Romagna, Modena, Italy 

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Abstract

Background: Few studies have investigated the independent health effects of different size fractions of particulate matter (PM), in multiple locations, especially in Europe.

Objectives: We estimated the short-term effects of PM with aerodynamic diameter less than 10μm (PM₁₀), less than 2.5μm (PM_2.5), and between 2.5 and 10μm (PM_2.5-10) on all-cause, cardiovascular and respiratory mortality in 10 European Mediterranean metropolitan areas within the MED-PARTICLES project.

Methods: We analyzed data from each city using Poisson regression models, and combined city-specific estimates to derive overall effect estimates. We evaluated the sensitivity of our estimates to co-pollutant exposures and city-specific model choice, and investigated effect modification by age, sex, and season. We applied distributed lag and threshold models to investigate temporal patterns of associations.

Results: A 10-μg/m³ increase in PM_2.5 was associated with a 0.55% (95% CI: 0.27, 0.84%) increase in all-cause mortality (0–1 day cumulative lag), and a 1.91% increase (95%CI: 0.71, 3.12%) in respiratory mortality (0–5 day lag). In general, associations were stronger for cardiovascular and respiratory mortality than all-cause mortality, during warm versus cold months, and among those ≥ 75 versus <75 years of age. Associations with PM_2.5-10 were positive but not statistically significant in most analyses, while associations with PM₁₀ seemed to be driven by PM_2.5

Conclusions: We found evidence of adverse effects of PM_2.5 on mortality outcomes in the European Mediterranean region. Associations with PM_2.5-10 were positive but smaller in magnitude. Associations were stronger for respiratory mortality when cumulative exposures were lagged over 0-5 days, and were modified by season and age.

Citation: Samoli E, Stafoggia M, Rodopoulou S, Ostro B, Declercq C, Alessandrini E, Díaz J, Karanansiou A, Kelessis AG, Le Tertre A, Pandolfi P, Randi G, Scarinzi C, Zauli-Sajani S, Katsouyanni K, Forastiere F, the MED-PARTICLES Study group. Environ Health Perspect (): .doi:10.1289/ehp.1206124

Received: October 11, 2012; Accepted: May 16, 2013; Published: May 17, 2013

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¹Center for Environmental Research and Children’s Health (CERCH), School of Public Health, University of California at Berkeley, Berkeley, California, USA; ²Department of Laboratory Medicine, University of Milano-Bicocca, School of Medicine, Hospital of Desio, Desio-Milano, Italy; ³School of Public Health, State University of New York, Albany, New York, USA

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Abstract

Background: In animal studies, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alters glucose transport and increases lipids and blood pressure. Epidemiologic evidence suggests an association between TCDD and metabolic disease.

Objectives: On July 10, 1976, a chemical explosion in Seveso, Italy, resulted in the highest known residential exposure to TCDD. Using data from the Seveso Women’s Health Study (SWHS), a cohort study of the health of the women, we examined the relation of serum TCDD to diabetes, metabolic syndrome, and obesity over 30 years later.

Methods: In 1996, we enrolled 981 women who were newborn to 40 years in 1976 and resided in the most contaminated areas. Individual TCDD concentration was measured in archived serum collected soon after the explosion. In 2008, 833 women participated in a follow-up study. Diabetes was classified based on self-report or fasting serum glucose and glycated hemoglobin levels. Metabolic syndrome was defined by International Diabetes Federation criteria. Obesity was defined as body mass index ≥30 kg/m².

Results: A 10-fold increase in serum TCDD (log₁₀TCDD) was not associated with diabetes (adjusted hazard ratio = 0.76; 95% confidence interval (CI): 0.45, 1.28) or obesity (adjusted odds ratio = 0.80; 95% CI: 0.58, 1.10). Log₁₀TCDD was associated with metabolic syndrome, but only among women who were ≤ 12 years at explosion (adjusted odds ratio = 2.03; 95% CI: 1.25, 3.29; p-interaction = 0.01).

Conclusions: We found an increase in metabolic syndrome associated with TCDD, but only among women who were youngest at exposure. Continued follow-up of the SWHS cohort will be informative.

Citation: Warner M, Mocarelli P, Brambilla P, Wesselink A, Samuels S, Signorini S, Eskenazi B. Environ Health Perspect (): .doi:10.1289/ehp.1206113

Received: October 08, 2012; Accepted: May 13, 2013; Published: May 14, 2013

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¹Department of Environmental Science, Policy and Management, University of California, Berkeley, California, USA; ²School of Public Health, University of California, Berkeley, California, USA; ³Energy & Resources Group, University of California, Berkeley, California, USA

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Abstract

Objective: To examine the distribution of heat risk-related land cover (HRRLC) characteristics across racial/ethnic groups and degrees of residential segregation.

Methods: Block group-level tree canopy and impervious surface estimates were derived from the 2001 National Land Cover Dataset for densely populated urban areas of the United States and Puerto Rico, and linked to demographic characteristics from the 2000 Census. Racial/ethnic groups in a given block group were considered to live in HRRLC if at least half their population experienced the absence of tree canopy and at least half of the ground covered by impervious surface (roofs, driveways, sidewalks, roads). Residential segregation was characterized for metropolitan areas in the United States and Puerto Rico using the multigroup dissimilarity index.

Results: After adjusting for ecoregion and precipitation, and holding segregation level constant, non-Hispanic blacks were 52% more likely (95% confidence interval (CI): 37% to 69%), non-Hispanic Asians 32% more likely (95% CI: 18% to 47%), and Hispanics 21% more likely (95% CI: 8% to 35%) to live in HRRLC conditions compared to non-Hispanic whites. Within each racial/ethnic group, HRRLC conditions increased with increasing degrees of metropolitan area-level segregation. Further adjustment for home ownership and poverty did not substantially alter these results, but adjustment for population density and metropolitan area population attenuated the segregation effects, suggesting a mediating or confounding role.

Conclusions: Land cover was associated with segregation within each racial/ethnic group, which may be partially explained by the concentration of racial/ethnic minorities into densely populated neighborhoods within larger, more segregated cities. In anticipation of greater frequency and duration of extreme heat events, climate change adaptation strategies, such as planting trees in urban areas, should explicitly incorporate an environmental justice framework that addresses racial/ethnic disparities in HRRLC.

Citation: Jesdale BM, Morello-Frosch R, Cushing L. Environ Health Perspect (): .doi:10.1289/ehp.1205919

Received: August 21, 2012; Accepted: April 30, 2013; Published: May 14, 2013

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¹Johns Hopkins Center for a Livable Future, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA; ²Department of Environmental Health Sciences, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA; ³Department of Health Policy and Management, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA; ⁴Institute of Chemistry, Karl-Franzens University, Graz, Austria; ⁵Department of Epidemiology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA

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Abstract

Background: Arsenic-based drugs are permitted in poultry production. Inorganic arsenic (iAs) causes cancer and maybe other adverse health outcomes. The contribution of chicken consumption to iAs intake, however, is unknown.

Objectives: To characterize arsenic species profile in chicken meat and estimate bladder and lung cancer risk associated with consuming chicken produced with arsenic-based drugs.

Methods: Conventional, conventional antibiotic-free, and organic chicken samples were collected from grocery stores in ten US metropolitan areas from December 2010 to June 2011. 116 raw and 142 cooked samples were tested for total arsenic, and 78 samples ≥10µg/kg dry weight underwent speciation.

Results: Total arsenic geometric mean (GM) in cooked chicken meat samples was 3.0 µg/kg (95% CI: 2.5, 3.6). Among 78 cooked samples that were speciated, iAs concentrations were higher in conventional samples (GM = 1.8 µg/kg; 95% CI: 1.4, 2.3) than antibiotic-free (GM = 0.7 µg/kg; 95% CI: 0.5, 1.0) or organic (GM = 0.6 µg/kg; 95% CI: 0.5, 0.8) samples. Roxarsone was detected in 20 of 40 conventional samples, one of 13 antibiotic-free samples, and none of the 25 organic samples. iAs concentrations in roxarsone-positive samples (GM = 2.3 µg/kg; 95% CI: 1.7, 3.1) were significantly higher than in roxarsone-negative samples (GM = 0.8 µg/kg; 95% CI: 0.7, 1.0). Cooking increased iAs and decreased roxarsone concentrations. Compared to organic chicken consumers, we estimated that conventional chicken consumers would ingest an additional 0.11µg/day iAs (in an 82g serving). Assuming lifetime exposure and a proposed cancer slope factor of 25.7 (mg kgBW^-1 day^-1)^-1, this could result in 3.7 extra lifetime bladder and lung cancer cases per 100,000 exposed-persons.

Conclusions: Conventional chicken meat had higher iAs concentrations than conventional antibiotic-free and organic chicken meat samples. Cessation of arsenical drug use could reduce exposure and the burden of arsenic-related disease in chicken consumers.

Citation: Nachman KE, Baron PA, Raber G, Francesconi KA, Navas-Acien A, Love DC. Environ Health Perspect (): .doi:10.1289/ehp.1206245

Received: November 08, 2012; Accepted: April 16, 2013; Published: May 11, 2013

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¹Institute of Environmental Medicine, Unit of Metals and Health, Karolinska Institutet, Stockholm, Sweden; ²Department of Laboratory Medicine, Section of Occupational and Environmental Medicine, Lund University, Lund, Sweden; ³Swedish National Food Agency, Risk-benefit assessment department, Uppsala, Sweden; ⁴Hospital Dr. Nicolás Cayetano Pagano, San Antonio de los Cobres, Argentina

Advance Publication

Abstract

Background: In humans, inorganic arsenic is metabolized to methylated metabolites mainly by arsenic (+3 oxidation state) methyltransferase (AS3MT). AS3MT polymorphisms are associated with arsenic metabolism efficiency. Recently, a putative N-6-Adenine-Specific DNA methyltransferase 1 (N6AMT1) was found to methylate arsenic in vitro.

Objective: To evaluate the role of N6AMT1 polymorphisms in arsenic methylation efficiency in humans.

Methods: We assessed arsenic methylation efficiency in 188 women exposed to arsenic via drinking water (about 200 µg/L) in the Argentinean Andes by measuring the relative concentrations of arsenic metabolites in urine [inorganic arsenic, methylarsonic acid (MMA), and dimethylarsinic acid] by HPLC-HG-ICPMS. We performed genotyping for N6AMT1 and AS3MT polymorphisms by Taqman assays, and gene expression (in blood; N=63) with Illumina HumanHT-12 v4.0.

Results: N6AMT1 SNPs (rs1997605, rs2205449, rs2705671, rs16983411, and rs1048546) and 2 N6AMT1 haplotypes were significantly associated with %MMA in urine, even after adjusting for AS3MT haplotype. %MMA increased monotonically according to the number of alleles for each SNPs, e.g, for rs1048546, mean % MMA was 7.5% for GG, 8.8% for GT, and 9.7% for TT carriers. Three SNPs were in linkage disequilibrium (R²>0.8). Estimated associations for joint effects of N6AMT1 (haplotype 1) and AS3MT (haplotype 2) were generally consistent with expectations for additive effects of each haplotype on %MMA. Carriers of N6AMT1 genotypes associated with lower %MMA showed the lowest N6AMT1 expression, but associations were monotonic according to copy number for only one genotype and one haplotype.

Conclusions: N6AMT1 polymorphisms were associated with arsenic methylation in Andean women, independent of AS3MT. N6AMT1 polymorphisms may be susceptibility markers for arsenic-related toxic effects.

Citation: Harari F, Engström K, Concha G, Colque G, Vahter M, Broberg K. Environ Health Perspect (): .doi:10.1289/ehp.1206003

Received: September 11, 2012; Accepted: May 08, 2013; Published: May 10, 2013

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¹Department of Population Health and Environmental Medicine, New York University School of Medicine, New York, New York, USA; ²Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York City, New York, USA; ³U-Chicago Research Bangladesh, Ltd., Dhaka, Bangladesh; ⁴Departments of Health Studies, Medicine and Human Genetics and Comprehensive Cancer Center, The University of Chicago, Chicago, Illinois, USA

Advance Publication

Abstract

Background: Prospective studies that evaluate the influence of arsenic methylation capacity on cardiovascular disease (CVD) risk are lacking.

Objective: To evaluate the association of arsenic exposure from drinking water and arsenic methylation capacity with CVD risk.

Method: We conducted a case-cohort study of 369 incident fatal and non-fatal cases of CVD, including 148 stroke cases and 211 cases of heart disease, and a subcohort of 1,109 subjects randomly selected from the 11,224 participants in the Health Effects of Arsenic Longitudinal Study.

Results: The adjusted hazard ratio (HR) for all CVD, heart disease, and stroke in association with a standard deviation increase in baseline well arsenic (112 µg/L) was 1.15 (95% CI: 1.01, 1.30), 1.20 (95% CI: 1.04, 1.38), and 1.08 (95% CI: 0.90, 1.30), respectively. Adjusted HRs for the second and third tertiles of urinary monomethylarsonic acid (MMA)% relative to the lowest tertile, respectively, were 1.27 (95% CI: 0.85, 1.90) and 1.55 (95% CI: 1.08, 2.23) for all CVD, and 1.65 (95% CI: 1.05, 2.60) and 1.61 (95% CI: 1.04, 2.49) for heart disease specifically. The highest versus lowest ratio of urinary dimethylarsinic acid (DMA) to MMA was associated with a significantly decreased risk of CVD (HR=0.54; 95% CI: 0.34, 0.85) and heart disease (HR=0.54; 95% CI: 0.33, 0.88). There was no apparent association between arsenic metabolite indices and stroke risk. The joint effects of incomplete arsenic methylation capacity, indicated by higher urinary MMA% or lower urinary DMA%, with higher levels of well arsenic on heart disease risk were additive. There was some evidence of a synergy of incomplete methylation capacity with older age and cigarette smoking.

Conclusions: Arsenic exposure from drinking water and incomplete methylation capacity of arsenic were adversely associated with heart disease risk.

Citation: Chen Y, Wu F, Liu M, Parvez F, Slavkovich V, Eunus M, Ahmed A, Segers S, Argos M, Islam T, Rakibuz-Zaman M, Hasan R, Sarwar G, Levy D, Graziano J, Ahsan H. Environ Health Perspect (): .doi:10.1289/ehp.1205797

Received: July 19, 2012; Accepted: May 08, 2013; Published: May 10, 2013

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¹London School of Hygiene and Tropical Medicine, London, UK; ²London International Development Centre, London, UK; ³London School of Hygiene and Tropical Medicine, London, UK; London School of Economics, London, UK; ⁴Royal Veterinary College, London, UK; ⁵Institute of Development Studies, University of Sussex, UK; ⁶Mahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand; ⁷Oxford University Clinical Research Unit, Hanoi, Vietnam; ⁸Imperial College, Centre for the History of Science, Technology, and Medicine, London, UK

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Abstract

Background: In many parts of the world, livestock production is undergoing a process of rapid intensification. The health implications of this development are uncertain. Intensification creates cheaper products, allowing more people to access animal-based foods. However, some practices associated with intensification may contribute to zoonotic disease emergence and spread, for example the sustained use of antibiotics, concentration of animals in confined units, and long distance and frequent movement of livestock.

Objectives: This paper reviews the diverse range of ecological, biological, and socio-economic factors likely to enhance or reduce zoonotic risk, and identifies why improved understanding requires an interdisciplinary approach. A conceptual framework is then offered to guide systematic research on this problem.

Discussion: We recommend that interdisciplinary work on zoonotic risk should be able to account for the complexity of risk environments, rather than simple linear causal relations between risk drivers and disease emergence and/or spread. Further, we recommend that interdisciplinary integration is needed at different levels of analysis, from the study of risk environments to the identification of policy options for risk management.

Conclusion: Given rapid changes in livestock production systems in developing countries and their potential health implications at the local and global level, the problem we analyse here is of great importance for environmental health and development. While we offer a systematic interdisciplinary approach to understand and address these implications, we recognise that further research is needed to clarify methodological and practical questions arising from the integration of the natural and social sciences.

Citation: Liverani M, Waage J, Barnett T, Pfeiffer DU, Rushton J, Rudge JW, Loevinsohn ME, Scoones I, Smith RD, Cooper BS, White LJ, Goh S, Horby P, Wren B, Gundogdu O, Woods A, Coker RJ. Environ Health Perspect (): .doi:10.1289/ehp.1206001

Received: September 10, 2012; Accepted: May 08, 2013; Published: May 10, 2013

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¹Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, New York, USA; ²Children’s Hospital Boston, Boston, Massachusetts, USA; ³Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA; ⁴Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA; ⁵Channing Laboratory, Brigham and Women’s Hospital & Harvard Medical School, Boston, Massachusetts, USA; ⁶Department of Preventive Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA; ⁷Mindich Child Health and Development Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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Abstract

Background: Ambient air pollution may have neurotoxic effects in children. Data examining associations between traffic-related air pollution and attention domains remain sparse.

Objectives: We examined associations between black carbon (BC), a marker of traffic particles, and attention measures ascertained at age 7-14 years among 174 children in a Boston-based birth cohort.

Methods: BC levels were estimated using a validated spatial-temporal land-use regression model based on residence during children’s lifetime. Children completed the Conner’s Continuous Performance Test (CPT) measuring omission errors, commission errors, and hit reaction time (HRT), with higher scores indicating increased errors or slower reaction time. Multivariable-adjusted linear regression analyses were used to examine associations between BC and each attention outcome.

Results: Children were primarily Hispanic (56%) and Caucasian (41%); 53% were boys. We found a positive association between higher BC levels with increased commission errors and slower HRT, adjusting for child IQ, age, gender, blood lead level, maternal education, pre- and postnatal tobacco smoke exposure, and community-level social stress. Notably, the association was weaker, though still positive, for the highest BC quartile relative to the middle two quartiles. Gender-stratified analysis demonstrated statistically significant associations between BC and both commission errors and HRT in boys, but BC was not significantly associated with any of the CPT outcomes in girls.

Conclusions: In this population of urban children, we found associations between BC exposure and higher commission errors and slower reaction time. These associations were overall more apparent in boys than girls.

Citation: Chiu YH, Bellinger DC, Coull BA, Anderson S, Barber R, Wright RO, Wright RJ. Environ Health Perspect (): .doi:10.1289/ehp.1205940

Received: August 28, 2012; Accepted: May 01, 2013; Published: May 10, 2013

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¹Department of Building Science, School of Architecture, Tsinghua University, Beijing, China; ²Environmental and Occupational Health Sciences Institute, University of Medicine and Dentistry of New Jersey (UMDNJ)–Robert Wood Johnson Medical School and Rutgers University, Piscataway, New Jersey, USA; ³International Centre for Indoor Environment and Energy, Technical University of Denmark, Lyngby, Denmark

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Abstract

Background: Over the past two decades there has been a large migration of China’s population from rural to urban regions. At the same time residences in cities have changed in character from single story or low rise buildings to high rise structures constructed and furnished with many man-made materials. As a consequence, indoor exposures (to pollutants with outdoor and indoor sources) have changed significantly.

Objectives: In this commentary we briefly discuss the inferred impact that urbanization and modernization have had on indoor exposures and public health in China. We argue that growing adverse health costs associated with these changes are not inevitable, and we present steps that could be taken to reduce indoor exposures to harmful pollutants.

Discussion: As documented by China’s Ministry of Health, there have been significant increases in morbidity and mortality among urban residents over the past 20 years. Evidence suggests that the population’s exposure to air pollutants has contributed to increases in lung cancer, cardiovascular disease, pulmonary disease and birth defects. Whether a pollutant has an outdoor or indoor source, most exposure to the pollutant occurs indoors. Going forward, indoor exposures can be reduced by reducing the ingress of outdoor pollutants (while providing adequate ventilation with clean air), minimizing indoor sources of pollutants, updating government policies related to indoor pollution, and addressing indoor air quality during a building’s initial design. Such steps could lead to significant reductions in morbidity and mortality, greatly reducing the societal costs associated with pollutant derived ill-health.

Citation: Zhang Y, Mo J, Weschler CJ. Environ Health Perspect (): .doi:10.1289/ehp.1205983

Received: September 06, 2012; Accepted: April 23, 2013; Published: May 10, 2013

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