Changes in industrial air pollution and the onset of childhood asthma in Quebec, Canada.

Ambient air pollution has been associated with asthma onset and exacerbation in children. Whether improvement in air quality due to reduced industrial emissions has resulted in improved health outcomes such as asthma in some localities has usually been assessed indirectly with studies on between-subject comparisons of air pollution from all sources and health outcomes. In this study we directly assessed, within small areas in the province of Quebec (Canada), the influence of changes in local industrial fine particulate matter (PM2.5), nitrogen dioxide (NO2), and sulfur dioxide (SO2) concentrations, on changes in annual asthma onset rates in children (≤12 years old) with a longitudinal ecological design. We identified the yearly number of new cases of childhood asthma in 1282 small areas (census tracts or local community service centers) for the years 2002, 2004, 2005, 2006, and 2015. Annual average concentrations of industrial air pollutants for each of the geographic areas, and three sectors (i.e., pulp and paper mills, petroleum refineries, and metal smelters) were estimated by the Polair3D chemical transport model. Fixed-effects negative binomial models adjusted for household income were used to assess associations; additional adjustments for environmental tobacco smoke, background pollutant concentrations, vegetation coverage, and sociodemographic characteristics were conducted in sensitivity analyses. The incidence rate ratios (IRR) for childhood asthma onset for the interquartile increase in total industrial PM2.5, NO2, and SO2 were 1.016 (95% confidence interval, CI: 1.006-1.026), 1.063 (1.045-1.090), and 1.048 (1.031-1.080), respectively. Positive associations were also found with pollutant concentrations from most individual sectors. Results suggest that changes in industrial pollutant concentrations influence childhood asthma onset rates in small localities.

Exposure to ultrafine particles and the incidence of asthma in children: A population-based cohort study in Montreal, Canada.

Asthma is the most prevalent chronic respiratory disease in children. The role of ultrafine particles (UFPs) in the development of the disease remains unclear. We used a population-based birth cohort to evaluate the association between prenatal and childhood exposure to low levels of ambient UFPs and childhood-onset asthma. Methods: The cohort included all children born and residing in Montreal, Canada, between 2000 and 2015. Children were followed for asthma onset from birth until <13 years of age. Spatially resolved annual mean concentrations of ambient UFPs were estimated from a land use regression model. We assigned prenatal exposure according to the residential postal code at birth. We also considered current exposure during childhood accounting for time-varying residence location. We estimated hazard ratios (HRs) using Cox proportional hazards models adjusted for age, sex, neighborhood material and social deprivation, calendar year, and coexposure to ambient nitrogen dioxide (NO2) and fine particles (PM2.5). Results: The cohort included 352,966 children, with 30,825 children developing asthma during follow-up. Mean prenatal and childhood UFP exposure were 24,706 particles/cm3 (interquartile range [IQR] = 3,785 particles/cm3) and 24,525 particles/cm3 (IQR = 3,427 particles/cm3), respectively. Both prenatal and childhood UFP exposure were not associated with childhood asthma onset in single pollutant models (HR per IQR increase of 0.99 [95% CI = 0.98, 1.00]). Estimates of association remained similar when adjusting for coexposure to ambient NO2 and PM2.5. Conclusion: In this population-based birth cohort, childhood asthma onset was not associated with prenatal or childhood exposure to low concentrations of UFPs.

Evolution in Trends of Primary Lower-Extremity Amputations Associated With Diabetes or Peripheral Artery Disease From 2006 to 2019.

BACKGROUND: Given the importance in prevention of lower extremity amputations (LEAs) associated with diabetes or peripheral artery disease (PAD), we sought to document the trends of primary LEA in Québec, Canada, from years 2006 to 2019. METHODS: Using the Québec Integrated Chronic Disease Surveillance System, we calculated crude and age-standardized annual incidence rates of primary LEA associated with diabetes and PAD among adults ≥ 40 years (99% confidence intervals [CI]), and all-cause 1-year mortality proportion trends following a primary LEA (95% CI), stratified by minor or major as the highest level of LEA during the same hospital stay and age groups. Trends were assessed using multivariate regression models. RESULTS: In 2019, the crude rate of primary LEA was 116.0 per 100,000 (n = 825) with 93.7 and 21.9 per 100,000 of minor (n = 665) and major (n = 160) LEA, respectively. A tendency of decrease by 8% (-15.0 to 0.4%) of age-standardized incidence of primary LEA was observed between 2006 and 2019, while the absolute number of primary LEA increased from 610 to 825 cases. Minor LEA increased by 14.2% (3.7 to 25.9%) and major LEA decreased by 49.5% (-57.1 to -40.5%). Incidence trends remained stable among the 40 to 64 years, and declined by 14.6% and 20.1% for the 65 to 79 and ≥ 80 years of age groups, respectively. Major LEA decreased in all age groups, whereas minor LEA increased by 26.2% among the patients 40 to 64 years of age only. Age-standardized 1-year mortality decreased by 35.1% (95% CI, -43.4 to -25.7%) between 2006 and 2019, with a crude 1-year mortality of 11.3% in 2019. CONCLUSIONS: The reduction of major LEA and 1-year mortality are encouraging, although increased minor LEA, especially in younger age groups, emphasizes the importance to improve preventive care further.

Long-term exposure to fine particulate matter and ozone and the onset of systemic autoimmune rheumatic diseases: an open cohort study in Quebec, Canada.

OBJECTIVES: To estimate associations between fine particulate matter (PM2.5) and ozone and the onset of systemic autoimmune rheumatic diseases (SARDs). METHODS: An open cohort of over 6 million adults was constructed from provincial physician billing and hospitalization records between 2000 and 2013. We defined incident SARD cases (SLE, Sjogren's syndrome, scleroderma, polymyositis, dermatomyositis, polyarteritis nodosa and related conditions, polymyalgia rheumatic, other necrotizing vasculopathies, and undifferentiated connective tissue disease) based on at least two relevant billing diagnostic codes (within 2 years, with at least 1 billing from a rheumatologist), or at least one relevant hospitalization diagnostic code. Estimated PM2.5 and ozone concentrations (derived from remote sensing and/or chemical transport models) were assigned to subjects based on residential postal codes, updated throughout follow-up. Cox proportional hazards models with annual exposure levels were used to calculate hazard ratios (HRs) for SARDs incidence, adjusting for sex, age, urban-versus-rural residence, and socioeconomic status. RESULTS: The adjusted HR for SARDS related to one interquartile range increase in PM2.5 (3.97 µg/m3) was 1.12 (95% confidence interval 1.08-1.15), but there was no clear association with ozone. Indirectly controlling for smoking did not alter the findings. CONCLUSIONS: We found associations between SARDs incidence and PM2.5, but no relationships with ozone. Additional studies are needed to better understand interplays between the many constituents of air pollution and rheumatic diseases.

Determination of a guidance value for the communication of individual-level biomonitoring data for urinary arsenic.

BACKGROUND: Available guidance values to interpret individual-level biomonitoring data (ILBD) for the sum of urinary inorganic-related arsenic species (SUIAS) are generally based on population statistical descriptors and not on a predetermined exposure level that should not be exceeded. The objective of this study was thus to propose a range of SUIAS concentrations, reflecting an exposure corresponding to WHO's provisional guideline value (PGV) for arsenic in drinking water (10 µg/L), within which an exposure-based biomonitoring guidance value can be identified. METHOD A comprehensive literature review was carried out in order to identify studies that were relevant to the determination of a guidance value. Drinking water arsenic exposure and urinary biomonitoring concentrations obtained from selected studies were used to conduct a structural equation modeling meta-analysis, from which regression coefficients were obtained to derive an interpretative guidance range. RESULTS Individuals exposed to the arsenic background level comparable to North American and European countries and to a water source contaminated at the WHO's PGV, would have, on average, urinary SUIAS between 9 and 20 µg/L, with the most probable value being 15 µg/L. To address the associated uncertainty, the final guidance value selection within this range may be based on a targeted sensitivity and specificity towards detecting overexposed individuals. Indeed, spans of sensitivity of 60-82%, and of specificity of 58-85%, were estimated for the proposed range based on drinking water exposure raw data from the literature. CONCLUSION The range of guidance values obtained appears suitable for interpreting and communicating ILBD in any population biomonitoring studies in which background exposure is comparable to the North American and European context. Before selecting a single value within the proposed range, it will be important for Public Health officials to assess the possible consequences of this selection on the management and communication of the biomonitoring results.

Blood mercury and plasma polychlorinated biphenyls concentrations in pregnant Inuit women from Nunavik: Temporal trends, 1992-2017.

The Inuit of Nunavik (Northern Quebec, Canada) are exposed to polychlorinated biphenyls (PCBs) and mercury (Hg) through their consumption of marine country foods. A temporal trend study was initiated in 1992 to monitor circulating levels of PCBs and Hg in pregnant Inuit women, since the fetus is most at risk of adverse health effects. We set out (1) to describe temporal trends of PCBs and Hg levels in pregnant Nunavik women between 1992 and 2017; (2) to determine the prevalence of participants exceeding the guidance values in 2017; (3) to investigate relations between marine country food intake and contaminant levels over the study period. A total of 559 pregnant women provided a blood sample for contaminant analysis from 1992 to 2017. PCB congeners were quantified in plasma (serum) by gas chromatography (GC) coupled to electron capture detection or mass spectrometry (MS). We determined whole blood mercury concentration by cold vapor atomic absorption or inductively-coupled plasma MS. We performed multilevel modeling to assess temporal trends in contaminant levels and relations with marine country food consumption. Concentrations of total PCBs and Hg decreased by 84% and 65% between 1992 and 2017, respectively. Nevertheless, 10% and 22% of women in 2017 exceeded guidance values for PCBs and Hg, respectively. While the decline in marine country food intake is the only factor associated with decreasing Hg levels, other factors may explain the decline in PCB levels. Despite the significant decline in PCBs and Hg levels from 1992 to 2017, exposure to these contaminants is still quite prevalent among pregnant Nunavik women. Most of the decline in Hg exposure is likely due to a shift away from marine country foods to store-bought foods, which is a concern given the cultural and nutritional importance of country foods and the high food insecurity that prevails in Nunavik.

Exposure to perfluoroalkyl substances (PFAS) and associations with thyroid parameters in First Nation children and youth from Quebec.

BACKGROUND: Perfluoroalkyl substances (PFASs) are found in several consumer goods. Exposure to PFASs in children has been associated with alteration in thyroid hormones, which have critical roles in brain function. OBJECTIVE: In 2015, 198 children and youth (3-19 y) were recruited as part of the pilot project Jeunes, Environnement et Santé/Youth, Environment and Health (JES!-YEH!), realized in collaboration with four First Nation communities in Quebec. We aimed to evaluate serum concentrations of PFASs in relation to concentrations of thyroid-stimulating hormone (TSH), free thyroxine (T4) and thyroglobulin while adjusting for relevant confounders. METHODS: PFASs (PFOS, PFOA, PFHxS, PFNA), 2,2',4,4'-Tetrabromodiphenyl ether (PBDE-47) thyroid parameters (TSH, free T4, and thyroglobulin) were measured in serum samples of 186 participants. Iodine, creatinine, and cotinine were measured in urine samples. Serum levels of PFASs were compared to those measured in the general Canadian population and elsewhere. Multivariate regression analyses were performed to determine associations between PFASs and TSH, free T4 and thyroglobulin. RESULTS: PFOS, PFOA and PFHxS serum concentrations were low. However, PFNA concentrations among participants aged 12 to 19 years old from Anishinabe communities were three times higher than those measured in the Canadian Health Measures Survey (2009-2011) for the same age group (Geometric Means: 3.01 µg/L and 0.71 µg/L, respectively) and were particularly higher in the Anishinabe participants aged 6 to 11 years old (GM: 9.44 µg/L). Few participants had levels of TSH, free T4, and thyroglobulin outside age-specific paediatric ranges. When adjusted for relevant covariates and other contaminants, PFNA serum concentrations were positively associated with free T4 levels (Adjusted ß = 0.36; p = 0.0014), but not with TSH and thyroglobulin levels. No association was observed between the other PFAS and thyroid hormones parameters. CONCLUSION: This pilot project reveals among the highest exposure to PFNA in children reported until today, and suggests effects of PFNA as an endocrine disruptor, highlighting the importance of investigating the sources and effects of disproportionate exposure to emerging contaminants in some indigenous communities and ban all PFAS at the international scale.

Socio-economic inequalities in blood mercury (Hg) and serum polychlorinated biphenyl (PCB) concentrations among pregnant Inuit women from Nunavik, Canada.

OBJECTIVE: We examined the relationships between socio-economic characteristics and mercury (Hg) and polychlorinated biphenyl (PCB) concentrations among pregnant Inuit women from Nunavik. METHOD: We used biomonitoring data from 208 pregnant Inuit women recruited in the 14 villages of Nunavik between September 2011 and December 2013. Blood samples were collected to monitor levels of blood Hg and serum congener PCB-153 (surrogate of total PCB concentration). Ratio of omega 3/omega 6 polyunsaturated fatty acids, a validated biomarker of marine country food consumption, was also measured in red blood cell membranes to determine maternal dietary profile. Data on socio-economic characteristics (income and education), health-related lifestyles, and reproductive history were collected through questionnaires. Association between socio-economic characteristics and contaminant concentrations was assessed using linear regressions. RESULTS: We observed a significant inverse relationship between education and Hg levels. Lower concentrations of Hg were observed among women who had completed high school compared to women who had not completed high school. However, no association was observed between level of education and concentration of PCBs. CONCLUSION: Socio-economic disparities in maternal exposure to Hg exist in Nunavik. Further research is needed to determine whether environmental health inequalities also exist in other subgroups of the Nunavik population and in other Indigenous communities in Canada.

Cardiovascular risk factors and subclinical atherosclerosis among Nunavik Inuit.

OBJECTIVE: To evaluate subclinical atherosclerosis in Nunavik Inuit and its correlation to traditional cardiovascular disease risk factor. METHOD: The intima-media thickness (IMT) of 12 segments of the carotid arteries (IMT(12_seg)) free of plaque were assessed in randomly selected 40 years old and older Inuit from. Clinical assessment was performed which included fasting plasma glucose, fasting insulin, systemic blood pressure, body mass index, smoking, circulating blood lipids and oral glucose tolerance test. In addition, documented presence of ischemic heart disease (IHD), stroke, diabetes mellitus, hypertension and dyslipidemia were determined from medical files. RESULTS: The average age of the 287 participants was 51.2 ± 0.6 years (56.8% women). Mean IMT(12_seg) was 0.80 ± 0.17 mm (range: 0.55-1.47 mm). Compared with disease free Inuit, individuals with history of stroke showed greater carotid internal IMT (0.68 ± 0.01 mm vs. 0.96 ± 0.15 mm respectively; p<0.005) but no difference was observed for IHD. Hypertensive and dyslipidemic Inuit had higher IMT(12_seg) compared to risk factor free individuals but no difference was observed in diabetics. None of the clinical assessments were associated with IMT(12_seg). In a multivariate backward elimination model, only age, gender, and medically documented history of hypertension were found to be predictors of IMT(12_seg) (adjusted r-square of 0.54; p<0.0001). CONCLUSION: Compared with disease free Nunavik Inuit, subclinical signs of atherosclerosis determined by IMT was higher in individual diagnosed with stroke. Independent predictors of IMT(12_seg) in our group were age, gender and history of hypertension. No other traditional risk factors imparted IMT.