Inorganic arsenic is a known human carcinogen and is routinely detected in US community water systems (CWSs). Inequalities in CWS arsenic exist across broad sociodemographic subgroups. Our objective was to evaluate the county-level association between socioeconomic vulnerability and CWS arsenic concentrations across the US. We evaluated previously developed, population-weighted CWS arsenic concentrations (2006–2011) and three socioeconomic domains (the proportion of adults with a high school diploma, median household income, and the Centers for Disease Control and Prevention's overall socioeconomic vulnerability score) for 2,604 conterminous US counties. We used spatial lag models and evaluated the adjusted geometric mean ratio (GMR) of CWS arsenic concentrations per higher socioeconomic domain score corresponding to the interquartile range, and also evaluated flexible quadratic spline models. We also stratified by region and by United States Department of Agriculture Rural-Urban Continuum Codes to assess potential effect measure modification by region and rurality. Associations between socioeconomic vulnerability and CWS arsenic were modified by region and rurality and specific to socioeconomic domain. The fully adjusted GMR (95% CIs) of CWS arsenic per interquartile range higher proportion of adults with a high school education was 0.83 (0.71, 0.98) in the Southwest (corresponding to 17% lower arsenic with higher education), 0.82 (0.71, 0.94) in the Eastern Midwest (18% lower), and 0.65 (0.31, 1.36) in New England (35% lower). Associations between median household income and CWS arsenic were largely null. Higher overall socioeconomic vulnerability was significantly associated with lower CWS arsenic, but only in counties in the Central Midwest and those with total populations less than 20,000. Findings may reflect regional/local differences in both socioeconomic/socio-cultural context and public drinking water regulatory efforts. Across the US, individual domains of socioeconomic vulnerability (especially educational attainment) are more strongly associated with inequalities in CWS arsenic than the complex overall socioeconomic vulnerability index.

Open waste burning emissions constitute a significant source of air pollution affecting human health in India. In regions where cleaner fuels have displaced solid biofuel usage, open waste burning is rapidly becoming one of the largest sources of airborne human class-I-carcinogens and particulate matter. As the establishment of waste management infrastructure in rural India is likely to take years, we explore whether health-relevant emissions can be reduced by legalizing the burning of dry non-biodegradable waste in improved devices. We measure the emission factors of 76 VOCs, CH₄, CO, and CO₂ from different types of waste burned in two different improved devices, a burn basket and a local water heater. Based on our experiments, we create four “what-if” intervention scenarios to assess the improvement of air quality due to the emission reductions that can be accomplished by four management strategies. We find that substituting the traditional, more polluting water heating fuels with dry plastic waste across rural India can reduce primary emissions (e.g., −29 Ggy⁻¹ for benzene) and ozone formation potential (−2960 Ggy⁻¹) from open waste burning. When dry waste is used in lieu of more polluting fuels, and its burning serves a purpose, the net class-I-carcinogen benzene emissions, would be halved compared to the present. The change in emissions for the class-I carcinogen 1,3-butadiene would become net negative. This happens because the emissions avoided when part of the solid biofuel currently used in rural India is replaced by plastic waste (4.1 (1.2–4.1) Ggy⁻¹) exceed the waste burning emissions of this compound (3 (1.2–3.7) Ggy⁻¹) by so much, that residential sector emission reductions offset all waste burning emissions including those of landfill fires. Our study demonstrates that India's air quality can be improved by permitting and promoting the use of dry packaging waste in lieu of traditional biofuels and by promoting improved burning devices.

Arsenic (As) is a ubiquitous environmental carcinogen that enters the human food chain mainly through rice grains. In the present study, we evaluated the potential of thiourea (TU; non-physiological reactive oxygen species scavenger) in mitigating the negative effects of arsenic (As) stress in indica rice variety IR64, with the overall aim to reduce grain As accumulation. At seedling stage, As + TU treatment induced the formation of more numerous and longer crown roots compared with As alone. The As accumulation in main root, crown root, lower leaf and upper leaf was significantly reduced to 0.1-, 0.14-, 0.16-, 0.14-fold, respectively in As + TU treated seedlings compared with those of As alone. This reduced As accumulation was also coincided with light-dependent suppression in the expression levels of aquaporins and photosynthesis-related genes in As + TU treated roots. In addition, the foliar-supplemented TU under As-stress maintained reducing redox conditions which decreased the rate of As accumulation in flag leaves and, eventually grain As by 0.53-fold compared with those of As treatment. The agronomic feasibility of TU was validated under naturally As contaminated sites of Nadia (West Bengal, India). The tiller numbers and crop productivity (kg seed/ha) of TU-sprayed plants were increased by 1.5- and 1.18-fold, respectively; while, grain As accumulation was reduced by 0.36-fold compared with those of water-sprayed control. Thus, this study established TU application as a sustainable solution for cultivating rice in As-contaminated field conditions.

The fate of organic pollutants in the environment, especially the formation and stability of non-extractable (i.e., bound) residues (NERs) determines their environmental risk. Using ¹⁴C-tracers, we studied the fate of the carcinogen phenanthrene in active or sterilized oxic loamy soil in the absence and presence of the geophagous earthworm Metaphire guillelmi and characterized the NERs derived from phenanthrene. After incubation of ¹⁴C-phenanthrene in active soil for 28 days, 40 ± 3.1% of the initial amount was mineralized and 70.1 ± 1.9% was converted to NERs. Most of the NERs (>92%) were bound to soil humin. Silylation of the humin-bound residues released 45.3 ± 5.3% of these residues, which indicated that they were physically entrapped, whereas the remainder of the residues were chemically bound or biogenic. By contrast, in sterilized soil, only 43.4 ± 12.6% of the phenanthrene was converted to NERs and all of these residues were completely released upon silylation, which underlines the essential role of microbial activity in NER formation. The presence of M. guillelmi in active soil significantly inhibited phenanthrene mineralization (24.4 ± 2.6% mineralized), but NER formation was not significantly affected. Only a small amount of phenanthrene-derived residues (1.9–5.3% of the initial amount) accumulated in the earthworm body. When humin-bound residues were mixed with fresh soil, 33.9% (humin recovered from active soils) and 12.4% (humin recovered from sterilized soils) of the residues were mineralized after 75 days of incubation, respectively, which indicated a high bioavailability of NERs, albeit lower than the initial addition of phenanthrene. Our results indicated that many phenanthrene-derived NERs, especially those physically entrapped, are still bioavailable and may pose a toxic threat to soil organisms.

Benzene exposure represents a potential risk for children's health. Apart from being a known carcinogen for humans (group 1 according to IARC), there is scientific evidence suggesting a relationship between benzene exposure and respiratory problems in children. But results are still inconclusive and inconsistent. This study aims to assess the determinants of exposure to indoor and outdoor residential benzene levels and its relationship with respiratory health in infants. Participants were 1-year-old infants (N = 352) from the INMA cohort from Valencia (Spain). Residential benzene exposure levels were measured inside and outside dwellings by means of passive samplers in a 15-day campaign. Persistent cough, low respiratory tract infections and wheezing during the first year of life, and covariates (dwelling traits, lifestyle factors and sociodemographic data) were obtained from parental questionnaires. Multiple Tobit regression and logistic regression models were performed to assess factors associated to residential exposure levels and health associations, respectively. Indoor levels were higher than outdoor ones (1.46 and 0.77 μg/m3, respectively; p < 0.01). A considerable percentage of dwellings, 42% and 21% indoors and outdoors respectively, surpassed the WHO guideline of 1.7 μg/m3 derived from a lifetime risk of leukemia above 1/100 000. Monitoring season, maternal country of birth and parental tobacco consumption were associated with residential benzene exposure (indoor and outdoors). Additionally, indoor levels were associated with mother's age and type of heating, and outdoor levels were linked with zone of residence and distance from industrial areas. After adjustment for confounding factors, no significant associations were found between residential benzene exposure levels and respiratory health in infants. Hence, our study did not support the hypothesis for the benzene exposure effect on respiratory health in children. Even so, it highlights a public health concern related to the personal exposure levels, since a considerable number of children surpassed the abovementioned WHO guideline for benzene exposure.

Within fossil- and solid-fuel dependent geographic locations, mechanisms of air pollution-induced asthma remains unknown. In particular, sources of greater genetic susceptibility to airborne carcinogen, namely, benzo[a]pyrene (B[a]P) has never been investigated beyond that of a few well known genes.To deepen our understanding on how the genotypic variations within the candidate genes contribute to the variability in the children's susceptibility to ambient B[a]P on doctor-diagnosed asthma.Clinically confirmed asthmatic versus healthy control children (aged, 7–15) were enrolled from historically polluted and rural background regions in Czech Republic. Contemporaneous ambient B[a]P concentration was obtained from the routine monitoring network. The sputum DNA was genotyped for 95 genes. B[a]P interaction with SNPs was studied by two-stage, semi-agnostic screening of 621 SNPs.The median B[a]P within the highly polluted urban center was 8-times higher than that in the background region (7.8 vs. 1.1 ng/m³) during the period of investigation. Within the baseline model, which considered B[a]P exposure-only, the second tertile range was associated with a significantly reduced odds (aOR = 0.28) of asthma (95% CI, 0.16 to 0.50) compared to those at the lowest range. However, the highest range of B[a]P was associated with 3.18-times greater odds of the outcome (95% CI, 1.77 to 5.71). Within the gene-environment interaction models, joint occurrence of a high B[a]P exposure range and having a high-risk genotype at CTLA4 gene (rs11571316) was associated with 9-times greater odds (95% CI, 4.56–18.36) of the asthma diagnosis. Similarly, rs11571319 at CTLA4 and a high B[a]P exposure range was associated with a 8-times greater odds (95% CI, 3.95–14.27) of asthma diagnosis. Furthermore, having TG + GG genotypes on rs1031509 near STAT4 was associated with 5-times (95% CI, 3.03–8.55) greater odds of asthma diagnosis at the highest B[a]P range, compared to the odds at the reference range. Also CYP2E1 AT + TT genotypes (rs2070673) was associated with 5-times (95% CI, 3.1–8.8) greater odds of asthma diagnosis at the highest B[a]P exposure.The children, who jointly experience a high B[a]P exposure (6.3–8.5 ng/m3) as well as susceptible genotypes in CTLA4 (rs11571316 and rs11571319), STAT4 (rs1031509), and CYP2E1 (rs2070673), respectively, are associated with a significantly greater odds of having doctor-diagnosed asthma, compared to those with neither risk factors.

Inorganic arsenic is a chronic exposure carcinogen. Analysis of UK baby rice revealed a median inorganic arsenic content (n = 17) of 0.11 mg/kg. By plotting inorganic arsenic against total arsenic, it was found that inorganic concentrations increased linearly up to 0.25 mg/kg total arsenic, then plateaued at 0.16 mg/kg at higher total arsenic concentrations. Inorganic arsenic intake by babies (4-12 months) was considered with respect to current dietary ingestion regulations. It was found that 35% of the baby rice samples analysed would be illegal for sale in China which has regulatory limit of 0.15 mg/kg inorganic arsenic. EU and US food regulations on arsenic are non-existent. When baby inorganic arsenic intake from rice was considered, median consumption (expressed as μg/kg/d) was higher than drinking water maximum exposures predicted for adults in these regions when water intake was expressed on a bodyweight basis. Median consumption of organic arsenic levels for UK babies from baby rice is above threshold considered safe.

Benzene is a common environmental carcinogen that induces leukemia. Studies suggest that metabolic disorder has a relationship with the toxicity of benzene. Pyruvate kinase M2 (PKM2) is a key rate-limiting enzyme in glycolysis. However, the upstream and downstream regulatory mechanisms of PKM2 in benzene-induced hematotoxicity and the therapeutic effects of targeting PKM2 in vivo are unclear. This study aims to provide insights into the new mechanism of benzene-induced hematotoxicity and reveal the therapeutic significance of targeting PKM2. Herein, we demonstrated that PKM2-dependent glycolysis contributes to benzene-induced hematotoxicity by regulating inflammation reaction. Mechanistically, acetylated proteomics revealed that 1,4-benzoquinone (1,4-BQ) induced acetylation of PKM2 at position K66, and this modification contributed to the increase of PKM2 expression and can be inhibited by inhibition of acetyltransferase GCN5. Meanwhile, the elevated PKM2 was shown to prompt the activation of nuclear phosphorylated Stat3 (p-Stat3) and IL17A. Clinically, pharmacological inhibition of PKM2 alleviated the blood toxicity induced by benzene, which was mainly characterized by an increase in routine blood parameters and improvement of hematopoietic imbalance. Besides, elevated PKM2 is a promising biomarker in people occupationally exposed to benzene. Overall, we identified PKM2/p-Stat3/IL-17A axis participates in the hematotoxicity of benzene, and targeting PKM2 has certain therapeutic implications in hematologic diseases.

The exposure of benzo [a]pyrene (BaP) in recent times is rather unavoidable than ever before. BaP emissions are sourced majorly from anthropogenic rather than natural provenance from wildfires and volcanic eruptions. A major under-looked source is via the consumption of foods that are deep-fried, grilled, and charcoal smoked foods (meats in particular). BaP being a component of poly aromatic hydrocarbons has been classified as a Group I carcinogenic agent, which has been shown to cause both systemic and localized effects in animal models as well as in humans; has been known to cause various forms of cancer, accelerate neurological disorders, invoke DNA and cellular damage due to the generation of reactive oxygen species and involve in multi-generational phenotypic and genotypic defects. BaP's short and accumulated exposure has been shown in disrupting the fertility of gamete cells. In this review, we have discussed an in-depth and capacious run-through of the various origins of BaP, its economic distribution and its impact as well as toxicological effects on the environment and human health. It also deals with a mechanism as a single compound and its ability to synergize with other chemicals/materials, novel sensitive detection methods, and remediation approaches held in the environment.