Individual-level studies with adjustment for important COVID-19 risk factors suggest positive associations of long-term air pollution exposure (particulate matter and nitrogen dioxide) with COVID-19 infection, hospitalisations and mortality. The evidence, however, remains limited and mechanisms unclear. We aimed to investigate these associations within UK Biobank, and to examine the role of underlying chronic disease as a potential mechanism. UK Biobank COVID-19 positive laboratory test results were ascertained via Public Health England and general practitioner record linkage, COVID-19 hospitalisations via Hospital Episode Statistics, and COVID-19 mortality via Office for National Statistics mortality records from March–December 2020. We used annual average outdoor air pollution modelled at 2010 residential addresses of UK Biobank participants who resided in England (n = 424,721). We obtained important COVID-19 risk factors from baseline UK Biobank questionnaire responses (2006–2010) and general practitioner record linkage. We used logistic regression models to assess associations of air pollution with COVID-19 outcomes, adjusted for relevant confounders, and conducted sensitivity analyses. We found positive associations of fine particulate matter (PM₂.₅) and nitrogen dioxide (NO₂) with COVID-19 positive test result after adjustment for confounders and COVID-19 risk factors, with odds ratios of 1.05 (95% confidence intervals (CI) = 1.02, 1.08), and 1.05 (95% CI = 1.01, 1.08), respectively. PM 2.5 and NO 2 were positively associated with COVID-19 hospitalisations and deaths in minimally adjusted models, but not in fully adjusted models. No associations for PM₁₀ were found. In analyses with additional adjustment for pre-existing chronic disease, effect estimates were not substantially attenuated, indicating that underlying chronic disease may not fully explain associations. We found some evidence that long-term exposure to PM₂.₅ and NO₂ was associated with a COVID-19 positive test result in UK Biobank, though not with COVID-19 hospitalisations or deaths.

In the general population, chronic exposure to low-dose persistent organic pollutants (POPs), particularly organochlorine pesticides (OCPs), has been recently linked to many chronic diseases. Widespread contamination of the food chain and human adipose tissue has made avoiding exposure to these chemicals impossible; thus, alternative strategies for decreasing the chemical burden must be investigated. Recently, macronutrient intake was found to significantly modify the toxicokinetics of POPs in animal experimental studies. Thus, we evaluated whether macronutrient intake was related to serum concentrations of OCPs in healthy adults without cardio-metabolic diseases. Subjects included 1,764 adults, aged 20 years or above, who participated in the National Health and Nutrition Examination Survey 1999–2004. Macronutrient intake was assessed based on a 24-h dietary recall interview. Six individual OCPs commonly detected among the general population were evaluated as markers of OCPs and other coexisting lipophilic chemicals stored in adipose tissue and released into circulation. High fat intake was associated with lower concentrations of OCPs, while high carbohydrate intake showed the opposite result. When three types of fats were individually evaluated, both saturated fatty acids and monounsaturated fatty acids, but not polyunsaturated fatty acids, were inversely associated with serum concentrations of OCPs. Adjustment for possible confounders did not change the results. When stratified by age, gender, body mass index, and physical activity, these associations were similar in most subgroups. Thus, similar to the findings observed in animal experimental studies, a moderate-fat diet with low carbohydrate intake was related to low serum concentrations of OCPs in humans. Although these findings need to be replicated, changing dietary macronutrient intake can be investigated as a practical strategy for dealing with unavoidable lipophilic chemical mixtures such as OCPs in modern society.

Perfluoroalkyl substances (PFAS) are a diverse class of manufactured compounds used in a wide range of industrial processes and consumer products and have been detected in human serum worldwide. Previous cross-sectional and cohort studies in humans have suggested exposure to PFAS is associated with a wide array of chronic diseases, including endocrine disruption, developmental health effects, cancer and metabolic changes. We examined the associations between a panel of eight PFAS and indicators of thyroid disruption, kidney function, and body mass index (BMI), all of which were measured at repeated time points (1990–2008) over the course of the study. Participants (N = 210) were selected from the Fernald Community Cohort based on household water supply from a PFAS-contaminated aquifer. In adjusted repeated measures models, we observed several notable associations between serum PFAS and thyroid hormones as well as kidney function as measured by estimated glomerular filtration rate (eGFR). An interquartile (IQR) increase in serum PFOS was associated with a 9.75% (95% CI = 1.72, 18.4) increase in thyroid stimulating hormone. An IQR increase in serum PFNA, PFHxS, and PFDeA was associated with a −1.61% (95% CI = −3.53, −0.59), −2.06% (95% CI = −3.53, −0.59), and −2.20% (95% CI = −4.25, −0.14) change in eGFR, respectively. On the other hand, an IQR increase in serum Me-PFOSA was associated with a 1.53% (95% CI = 0.34, 2.73) increase in eGFR. No significant associations with BMI and serum PFAS were noted. Our findings are in agreement with previous reports that serum PFAS are associated with altered kidney and thyroid function.

Certain viruses and parasites can cause persistent infections that often co-occur and have been associated with substantial morbidity and mortality. Separate lines of research indicate exposures to per- and polyfluoroalkyl substances (PFAS) suppress the immune system. We hypothesized that PFAS exposures might systematically increase susceptibility to persistent infections resulting in a higher pathogen burden. We used data from 8778 individuals (3189 adolescents, 5589 adults) in the nationally-representative U.S. National Health and Nutrition Examination Survey (NHANES) 1999–2016 to examine cross-sectional associations between serum concentrations of four highly detected PFAS (PFOS, PFOA, PFHxS, PFNA) with the presence of antibodies to cytomegalovirus, Epstein Barr virus, hepatitis C and E, herpes simplex 1 and 2, HIV, T. gondii, and Toxocara spp. Seropositivity was summed to calculate a pathogen burden score reflecting the total number of infections. Separate survey-weighted multivariable regression models were fitted to analyze PFAS individually and quantile g-computation was used to analyze PFAS mixtures. Among adolescents, 38.7% had at least one persistent infection while 14.9% had two or more; among adults, these percentages were 48.0% and 19.7%. Each PFAS was individually associated with significantly higher pathogen burdens and the most pronounced associations were observed in adolescents [e.g., among adolescents, a doubling of PFOS was associated with 30% (95% CI: 25–36%) higher pathogen burden]. Quantile g-computation revealed PFAS mixtures as a whole were also associated with higher pathogen burdens. Taken together, these results suggest PFAS exposure may increase susceptibility to and foster the clustering of persistent infections, particularly among adolescents. Since persistent infections are important contributors to long-term health, prospective data are needed to confirm these findings.

Mining activities change the chemical composition of the environment and have negative reflection on people’s health and there is no single measure to deal with adverse consequences of mining activities, as each case is specific and needs to be understood and mitigated in a unique way. In this study, the combination of compositional data analysis (CoDA), k-means algorithm, hierarchical cluster analysis applied to reveal the geochemical associations of potentially toxic elements (PTE) in soil of Alaverdi city (Armenia) (Ti, Fe, Ba, Mn, Co, V, Pb, Zn, Cu, Cr, Mo, As). Additionally, to assess PTE-induced health risk, two commonly used approaches were used. The obtained results show that the combination of CoDA and machine learning algorithms allow to identify and describe three geochemical associations of the studied elements: the natural, manmade and hybrid. Moreover, the revealed geochemical associations were linked to the natural pattern of distribution of the element concentrations including the influence of the natural mineralization of the parent rocks, as well as the emission from the copper smelter and urban management related activities. The health risk assessment using the US EPA method demonstrated that the observed contents of studied elements are posing a non-carcinogenic risk to children in the entire territory of the city. In the case of adults, the non-carcinogenic risk was identified in areas situated close to the copper smelter. The Summary pollution index (Zc) values were in line with the results of the US EPA method and indicated that the main residential part of the city was under the hazardous pollution level suggesting the possibility of increase in the overall incidence of diseases among frequently ill individuals, children with chronic diseases and functional disorders of vascular system. The obtained results indicated the need for further in-depth studies with special focus on the synergic effect of PTE.

We performed a time series analysis to investigate the potential association between exposure to ambient air pollution and type 2 diabetes (T2D) incidence in the Chinese population. Monthly time series data between 2008 and 2015 on ambient air pollutants and incident T2D (N = 25,130) were obtained from the Environment Monitoring Center of Ningbo and the Chronic Disease Surveillance System of Ningbo. Relative risks (RRs) and 95% confidence intervals (95% CIs) of incident T2D per 10 μg/m³ increases in ambient air pollutants were estimated from Poisson generalized additive models. Exposure to particulate matter < 10 μm (PM₁₀) and sulfur dioxide (SO₂) was associated with increased T2D incidence. The relative risks (RRs) of each increment in 10 μg/m³ of PM₁₀ and SO₂ were 1.62 (95% CI, 1.16–2.28) and 1.63 (95% CI, 1.12–2.38) for overall participants, whereas for ozone (O₃) exposure, the RRs were 0.78 (95% CI, 0.68–0.90) for overall participants, 0.78 (95% CI, 0.69–0.90) for males, and 0.78 (95% CI, 0.67–0.91) for females, respectively. Exposure to PM₁₀ and SO₂ is positively associated with T2D incidence, whereas O₃ is negatively associated with T2D incidence.

Little evidence has demonstrated the association between health conditions and cooking water. The purpose of this study was to explore the relationship, using a representative sample of 10,531 subjects selected from the China Family Panel Study (CFPS). The usage rate of surface-exposed water showed a slight upward trend from 2010 to 2018. The adjusted odds ratio (OR) of chronic diseases with surface-exposed and well water was 1.140 (95% CI: 0.989–1.315) and 0.902 (95% CI: 0.839–0.969), respectively, with reference to tap/purified water. Surface-exposed water increased the likelihood of a worsening health change by 25.5% (OR: 1.255; 95% CI: 1.123–1.411), while well water was associated with poor self-rated health (OR: 1.169; 95% CI: 1.094–1.249). As such, surface-exposed water was associated with chronic diseases and worsening changes in health, and well water was negatively associated with chronic diseases. Although efforts to improve quality of drinking water have been made in China for decades, our conclusions reveal that water quality still remains a critical public livelihood issue among middle-aged and elderly populations. More in-depth research is required on whether the disinfection ingredients of tap water may increase the risk for chronic disease.

Air pollutants’ effect on ischemic stroke (IS) has been widely reported. But the effect of high-level concentrations during people’s outdoor periods among hypertension patients was unknown. Peak-hour concentrations were defined considering air pollutants’ high concentrations as well as people’s outdoor periods. We conducted a time-series study and used the generalized additive model to analyze peak-hour concentrations’ acute effect. A total of 315,499 IS patients comorbid with hypertension were admitted to secondary and above hospitals in Beijing from 2014 to 2018. A 10 µg/m³ (CO: 1 mg/m³) increase of the peak-hour concentrations was positively associated with IS hospital admissions among hypertension patients. The maximum effect sizes were as follows: for PM₂.₅, 0.17% (95% confidence interval [CI]: 0.10–0.24%) at Lag0 and 0.22% (95% CI: 0.12–0.33%) at Lag0–5; for PM₁₀, 0.09% (95% CI: 0.05–0.13%) at Lag5 and 0.17% (95% CI: 0.09–0.26%) at Lag0–5; for SO₂, 0.87% (95% CI: 0.46–1.29%) at Lag5; for NO₂, 0.83% (95% CI: 0.62–1.04%) at Lag0 and 0.86% (95% CI: 0.59–1.13%) at Lag0–1; for CO 1.23% (95% CI: 0.66–1.80%) at Lag0 and 1.33% (95% CI: 0.33–2.35%) at Lag0–5; for O₃ 0.23% (95% CI: 0.12–0.35%) at Lag0 and 0.20% (95% CI: 0.05–0.34%) at Lag0–1. The effect sizes of PM₂.₅, NO₂, and O₃ remained significant after adjusting daily mean. Larger effect sizes were observed for PM₂.₅ and PM₁₀ in cool season and for O₃ in warm season. As significant exposure indicators of air pollution, peak-hour concentrations exposure increased the risk of IS hospital admissions among hypertension patients and it is worthy of consideration in relative environmental standard. It is suggested for hypertension patients to avoid outdoor activity during peak hours. More relevant searches are required to further illustrate air pollutant’s effect on chronic disease population.

Air pollution is a worldwide health problem, and exposure to the pollution can cause damage to the human body, especially to the respiratory and cardiovascular systems. Asthma is the third most common chronic disease in Brazil, presenting high prevalence in some areas. The aim of this study was to evaluate the self-report the prevalence of asthma symptoms in Santos city, Brazil, and its associated factors in the adult population (between 18 and 59 years old). A cross-sectional study was applied in two different areas of the city. The participants of this study were selected by zip code estimated on a random sample. The ECHRS and a demographic questionnaire were used to collect data. Associations between categorical variables were tested using Pearson’s chi-square test or Fisher’s exact test. Single and multiple logistic regression models were applied to evaluate the risk factors for asthma. Georeferencing was implemented to distribute the cases. The highest prevalence of asthma was found in Ponta da Praia neighborhood (16.4%; p=0.019), as well as waking up with a coughing crisis in the last 12 months (26.4%; p <0.001). The risk factors for asthma were the following: living next Santos Port area (OR: 2.90; 95%CI 1.13–7.44); and the presence of O₃ (OR = 2.63; 95%CI 0.86–7.96). This pioneering study demonstrated that living near the port area increases the chances of adults having self-reported asthma symptoms.

Diabetes mellitus (DM) is a common chronic disease worldwide. Ambient air pollution has long been proven to be associated with type 2 diabetes mellitus (T2DM) progression, but the underlying mechanism is not clear yet. In addition, previous studies mainly focused on the prevention of healthy people against the incidence of T2DM. We designed a panel study including two follow-ups and enrolled 39 patients with T2DM living in Beijing. Linear mixed model was fitted to assess the association between two pairs of variables (ambient air pollution exposure and C3 levels, ambient air pollution exposures and T2DM index). Mediation analysis of C3 between ambient air pollution exposure and indicators of T2DM progression was conducted. We found that PM2.5 exposures is are negatively associated with serum complement C3. Given that C3 might act as a protector of pancreas β cell, PM2.5 exposures could accelerate disease in T2DM populations. No mediation effects were found. This study reveals that exposures to PM2.5 can cause progression of diseases among T2DM populations.