Association between toxic drug events and encephalopathy in British Columbia, Canada: a cross-sectional analysis.

BACKGROUND: Encephalopathy can occur from a non-fatal toxic drug event (overdose) which results in a partial or complete loss of oxygen to the brain, or due to long-term substance use issues. It can be categorized as a non-traumatic acquired brain injury or toxic encephalopathy. In the context of the drug toxicity crisis in British Columbia (BC), Canada, measuring the co-occurrence of encephalopathy and drug toxicity is challenging due to lack of standardized screening. We aimed to estimate the prevalence of encephalopathy among people who experienced a toxic drug event and examine the association between toxic drug events and encephalopathy. METHODS: Using a 20% random sample of BC residents from administrative health data, we conducted a cross-sectional analysis. Toxic drug events were identified using the BC Provincial Overdose Cohort definition and encephalopathy was identified using ICD codes from hospitalization, emergency department, and primary care records between January 1st 2015 and December 31st 2019. Unadjusted and adjusted log-binomial regression models were employed to estimate the risk of encephalopathy among people who had a toxic drug event compared to people who did not experience a toxic drug event. RESULTS: Among people with encephalopathy, 14.6% (n = 54) had one or more drug toxicity events between 2015 and 2019. After adjusting for sex, age, and mental illness, people who experienced drug toxicity were 15.3 times (95% CI = 11.3, 20.7) more likely to have encephalopathy compared to people who did not experience a drug toxicity event. People who were 40 years and older, male, and had a mental illness were at increased risk of encephalopathy. CONCLUSIONS: There is a need for collaboration between community members, health care providers, and key stakeholders to develop a standardized approach to define, screen, and detect neurocognitive injury related to drug toxicity.

Drug overdose and the risk of cardiovascular diseases: a nested case-control study.

BACKGROUND: North America has been experiencing an unprecedented epidemic of drug overdose. This study investigated the associations of drug overdose with the risk of cardiovascular disease (CVD) and 11 major CVD subtypes. METHODS: This nested case-control study was based on a cohort of 20% random sample of residents in British Columbia, Canada, who were aged 18-80 years and did not have known CVD at baseline (n = 617,863). During a 4-year follow-up period, persons who developed incident CVD were identified as case subjects, and the onset date of CVD was defined as the index date. For each case subject, we used incidence density sampling to randomly select up to five control subjects from the cohort members who were alive and did not have known CVD by the index date, were admitted to an emergency department or hospital on the index date for non-CVD causes, and were matched on age, sex, and region of residence. Overdose exposure on the index date and each of the previous 5 days was examined for each subject. RESULTS: This study included 16,113 CVD case subjects (mean age 53 years, 59% male) and 66,875 control subjects. After adjusting for covariates, overdose that occurred on the index date was strongly associated with CVD [odds ratio (OR), 2.9; 95% confidence interval (CI), 2.4-3.5], especially for arrhythmia (OR, 8.6; 95% CI, 6.2-12.0), ischemic stroke (OR, 5.3; 95% CI, 2.0-14.1), hemorrhagic stroke (OR, 3.1; 95% CI, 1.2-8.3), and myocardial infarction (OR, 3.0; 95% CI, 1.5-5.8). The CVD risk was decreased but remained significantly elevated for overdose that occurred on the previous day, and was not observed for overdose that occurred on each of the previous 2-5 days. CONCLUSIONS: Drug overdose appears to be associated with increased risk of cardiovascular diseases.

Spatial-temporal trends in the risk of illicit drug toxicity death in British Columbia.

BACKGROUND: Illicit drug poisoning (overdose) continues to be an important public health problem with overdose-related deaths currently recorded at an unprecedented level. Understanding the geographic variations in fatal overdose mortality is necessary to avoid disproportionate risk resulting from service access inequity. METHODS: We estimated the odds of fatal overdose per event from all cases captured by the overdose surveillance system in British Columbia (2015 - 2018), using both conventional logistic regression and Generalized Additive Models (GAM). The results of GAM were mapped to identify spatial-temporal trends in the risk of fatal overdose. RESULTS: We found that the odds of fatal overdose were about 30% higher in rural areas than in large urban centers, with some regions reporting odds 50% higher than others. Temporal variations in fatal overdose revealed an increasing trend over the entire province. However, the increase occurred earlier and faster in the Interior and Northern regions. CONCLUSION: Rural areas were disproportionately affected by fatal overdose; lack of access to harm reduction services may partly explain the elevated risk in these areas.

Risk of cardiovascular diseases in relation to substance use disorders.

BACKGROUND: Substance use disorder (SUD) has become increasingly prevalent worldwide, this study investigated the associations of SUD and alcohol, cannabis, opioid, or stimulant use disorder with cardiovascular disease (CVD) and 11 major CVD subtypes. METHODS: This study was based on a 20% random sample of residents in British Columbia, Canada, who were aged 18 - 80 years at baseline on January 1, 2015. Using linked administrative health data during 2010 - 2014, we identified people with various SUDs and prevalent CVDs at baseline, and examined the cross-sectional associations between SUDs and CVDs. After excluding people with CVDs at baseline, we followed the cohort for 4 years to identify people who developed incident CVDs, and examined the longitudinal associations between SUDs and CVDs. RESULTS: The cross-sectional analysis at baseline included 778,771 people (mean age 45 years, 50% male), 13,279 (1.7%) had SUD, and 41,573 (5.3%) had prevalent CVD. After adjusting for covariates, people with SUD were 2.7 (95% confidence interval [CI], 2.5 - 2.8) times more likely than people without SUD to have prevalent CVD. The longitudinal analysis included 617,863 people, 17,360 (2.8%) developed incident CVD during the follow-up period. After adjusting for covariates, people with SUD were 1.7 (95% CI, 1.6 - 1.9) times more likely than people without SUD to develop incident CVD. The cross-sectional and longitudinal associations were more pronounced for people with opioid or stimulant use disorder. CONCLUSIONS: People with SUD are more likely to have prevalent CVD and develop incident CVD compared with people without SUD.

Risk of overdose-related death for people with a history of incarceration.

BACKGROUND AND AIMS: Reported associations between previous incarceration and the risk of overdose-related death are substantially heterogeneous, and previous studies are limited by an inability to control for confounding factors in risk assessment. This study investigated the associations of overdose-related death with previous incarceration and the number or cumulative duration of previous incarcerations, and individual or neighborhood characteristics that may potentially modify the associations. DESIGN AND SETTING: A cohort study using a 20% random sample of residents in British Columbia, Canada. PARTICIPANTS: A total of 765 690 people aged 23 years or older at baseline as of 1 January 2015. Mean age was 50 years; 49% were males. MEASUREMENTS: Previous incarcerations that occurred during the 5-year exposure period (January 2010 to December 2014) were identified using provincial incarceration records. Overdose-related deaths that occurred during the 3-year follow-up period (January 2015 to December 2017) were identified using linked administrative health data. Baseline individual and neighborhood characteristics were retrieved from the provincial health insurance data. FINDINGS: In the cohort, 5743 people had an incarceration history during the exposure period, and 634 people died from drug overdose during the follow-up period. The mortality rate was 897 and 22 per 100 000 person-years for people who did and did not have an incarceration history, respectively. After adjusting for baseline individual and neighborhood characteristics (without any interaction term), people who had an incarceration history were 4.04 times (95% confidence interval 3.23-5.06) more likely to die from drug overdose compared with people without an incarceration history. The association was stronger for females, people without diagnoses of substance use disorder and people without dispensation of opioids for pain or benzodiazepines (P < 0.001 for each interaction term). There was no discernible linear trend between the number or cumulative duration of previous incarcerations and the risk of overdose-related death. CONCLUSIONS: Previous incarceration appears to be a major risk factor for overdose-related death.

Overdose and risk factors for coronavirus disease 2019.

BACKGROUND: There have been significant efforts to respond to the two public health emergencies of coronavirus disease 2019 (COVID-19) and overdose in British Columbia (BC), Canada. The purpose of this study was to quantify the prevalence of known risk factors associated with mortality due to COVID-19 for persons who have had a non-fatal overdose during 2015-2017 in comparison to persons who have not had an overdose. METHODS: Data were extracted from the BC Provincial Overdose Cohort which includes a 20 % random sample of BC residents and persons who have had a non-fatal overdose in BC from January 2015 to December 2017. Chi-square tests and logistic regression were used to compare risk factors by overdose history. RESULTS: Persons who had a non-fatal overdose were significantly more likely to have three (chronic pulmonary disease, diabetes, coronary heart disease) of the four known chronic conditions associated with the development of severe illness due to COVID-19 compared to persons who did not have a previous non-fatal overdose event. CONCLUSION: Persons who had an overdose were more likely to have several chronic conditions associated with the development of severe illness due to COVID-19. The increased likelihood of having these risk factors is reflective of the social and health inequities experienced by persons who have a history of overdose.

Snowfall, Temperature, and the Risk of Death From Myocardial Infarction: A Case-Crossover Study.

Previous research has associated snowfall with risk of myocardial infarction (MI). Most studies have been conducted in regions with harsh winters; it remains unclear whether snowfall is associated with risk of MI in regions with milder or more varied climates. A case-crossover design was used to investigate the association between snowfall and death from MI in British Columbia, Canada. Deaths from MI among British Columbia residents between October 15 and March 31 from 2009 to 2017 were identified. The day of each death from MI was treated as the case day, and each case day was matched to control days drawn from the same day of the week during the same month. Daily snowfall amount was assigned to case and control days at the residential address, using weather stations within 15 km of the residence and 100 m in elevation. In total, 3,300 MI case days were matched to 10,441 control days. Compared with days that had no snowfall, odds of death from MI increased 34% (95% confidence interval: 0%, 80%) on days with heavy snowfall (≥5 cm). In stratified analysis of deaths from MI as a function of both maximum temperature and snowfall, risk was significantly increased on snowfall days when the temperature was warmer.

Occupational Noise Exposure, Bilateral High-Frequency Hearing Loss, and Blood Pressure.

OBJECTIVE: The aim of this study was to investigate the relationships between occupational noise exposure and blood pressure using self-reported occupational exposure and bilateral high-frequency hearing loss. METHODS: This study included 4548 participants aged 20 to 69 years from the National Health and Nutrition Examination Survey 1999 to 2004. On the basis of self-reported exposure status, participants were divided into the current, former, or never exposed groups. Bilateral high-frequency hearing loss was defined as the average high-frequency hearing threshold at least 25 dB in both ears. RESULTS: The currently exposed participants had slightly increased diastolic blood pressure compared with those never exposed. Among previously exposed participants, those with bilateral high-frequency hearing loss had increased systolic blood pressure, heart rate, and the prevalence of hypertension compared with those with normal high-frequency hearing. CONCLUSION: Although there were some significant results, the evidence was not consistent to support the associations between occupational noise exposure and blood pressure.

Different types of housing and respiratory health outcomes.

Evidence has shown that housing conditions may substantially influence the health of residents. Different types of housing have different structures and construction materials, which may affect indoor environment and housing conditions. This study aimed to investigate whether people living in different types of housing have different respiratory health outcomes. The data from the 1999-2006 National Health and Nutrition Examination Survey were used for the analyses. The types of housing included houses, townhouses, apartments, and mobile homes. Respiratory symptoms included wheezing, coughing, sputum, and dyspnea; respiratory diseases included asthma, chronic bronchitis, emphysema, and chronic obstructive pulmonary disease (COPD). Multiple logistic regression was used to calculate odds ratio (OR) and 95% confidence interval (CI) after adjustment for potential confounding factors. A total of 11,785 participants aged 40 years and older were included in the analyses. Compared with those living in single family houses, participants living in mobile homes were more likely to have respiratory conditions, the OR (95% CI) was 1.38 (1.13-1.69) for wheezing, and 1.49 (1.25-1.78) for dyspnea; whereas participants living in apartments were less likely to have respiratory conditions, the OR (95% CI) was 0.58 (0.36-0.91) for chronic bronchitis, and 0.69 (0.49-0.97) for COPD. Compared with living in single family houses, living in mobile home was associated with worse, whereas living in apartments was associated with better, respiratory health outcomes. Further research is needed to better understand the underlying mechanisms and prevent adverse respiratory effects associated with living in mobile homes.

Association Between Overall and Mentholated Cigarette Smoking With Headache in a Nationally Representative Sample.

OBJECTIVE: The objective of this study was to determine associations between cigarette smoking and the existence of headache in a nationally representative sample, with attention to differences in effect estimates between mentholated and non-mentholated cigarettes smoking. METHODS: We examined cross-sectional associations between cigarette smoking and headache in 8,399 adults who participated in the National Health and Nutrition Examination Survey (NHANES) 1999-2004. The existence of headache was determined by an affirmative response to the question "During the past 3 months, did you have severe headaches or migraines?" Further refinement of headache diagnosis was not possible. We used logistic regression models to examine the association between cigarette smoking and headache. RESULTS: The current study included 8,399 participants aged 20 years and over, including 68% (n = 5491) never smokers and 32% (n = 2548) current smokers. Among the current smokers, 24% (n = 739) smoked menthol cigarettes, and 76% (n = 1719) smoked non-menthol cigarettes. Compared with never smokers, after adjustment for potential confounding factors, current smokers were more likely to have headache (OR: 1.38; 95% CI: 1.17-1.62; P < .001). With the increase of both the number of cigarettes smoked daily and pack-years of smoking, the likelihood of having headache was significantly increased compared with never smokers (P for linear trend < .001). Compared with non-mentholated smokers, mentholated smokers were not more likely to have headache (P = .302). CONCLUSIONS: Based on a nationally representative sample, we found that cigarette smoking was associated with headache in an exposure-response manner. Mentholated cigarette smokers were not more likely to have headache compared to non-mentholated cigarette smokers.

Exposure to loud noise, bilateral high-frequency hearing loss and coronary heart disease.

OBJECTIVES: Bilateral high-frequency hearing loss is an indicator for chronic exposure to loud noise. This study aimed to examine the association between bilateral high-frequency hearing loss and the presence of coronary heart disease (CHD). METHODS: This study included 5223 participants aged 20-69 years who participated in the audiometry examination of the National Health and Nutrition Examination Survey 1999-2004. Bilateral high-frequency hearing loss was defined as the average high-frequency (3, 4 and 6 kHz) hearing threshold ≥25 dB in both ears. CHD was defined as self-reported diagnoses by doctors or other health professionals. RESULTS: Compared with those with normal high-frequency hearing, participants with bilateral high-frequency hearing loss were more likely to have CHD (OR 1.91; 95% CI 1.28 to 2.85) after adjustment for various covariates. This association was particularly strong for currently employed workers who were exposed to loud occupational noise (OR 4.23; 95% CI 1.32 to 13.55). For this subgroup, there was no significant association of CHD with unilateral high-frequency hearing loss, and unilateral or bilateral low-frequency hearing loss. Furthermore, there was no significant association of CHD with any types of hearing loss for participants who were not exposed to loud noise. Stratified analyses for participants exposed to loud noise showed that the observed association was particularly strong for those who were less than 50 years of age, less educated and current smokers. CONCLUSIONS: On the basis of an objective indicator for personal chronic exposure to loud noise, this study confirmed that exposure to loud occupational noise is associated with the presence of CHD.

Socioeconomic disparities in secondhand smoke exposure among US never-smoking adults: the National Health and Nutrition Examination Survey 1988-2010.

BACKGROUND: Secondhand smoke (SHS) is a leading preventable cause of illness, disability and mortality. There is a lack of quantitative analyses on socioeconomic disparities in SHS; especially, it is not known how socioeconomic disparities have changed in the past two decades in the USA. OBJECTIVES: To examine socioeconomic disparities and long-term temporal trends in SHS exposure among US never-smoking adults aged ≥20 years. METHODS: 15 376 participants from the National Health and Nutrition Examination Survey (NHANES) 1999-2010 were included in the analysis of socioeconomic disparities; additional 8195 participants from NHANES III 1988-1994 were included in the temporal trend analysis. SHS exposure was assessed using self-reported exposure in the home and workplace as well as using serum cotinine concentrations ≥0.05 ng/mL. Individual socioeconomic status (SES) was assessed using poverty-to-income ratio. RESULTS: During the period 1999-2010, 6% and 14% of participants reported SHS exposure in the home and workplace, respectively; 40% had serum cotinine-indicated SHS exposure. Individual SES was strongly associated with SHS exposure in a dose-response fashion; participants in the lowest SES group were 2-3 times more likely to be exposed to SHS compared with those in the highest SES group. During the period 1988-2010, the prevalence declined over 60% for the three types of SHS exposure. However, for cotinine-indicated exposure, the magnitudes of the declines were smaller for lower SES groups compared with higher SES groups, leading to widening socioeconomic disparities in SHS exposure. CONCLUSIONS: SHS exposure is still widespread among US never-smoking adults, and socioeconomic disparities for cotinine-indicated exposure have substantially increased in the past two decades.

Long-term exposure to traffic-related air pollution and progression of carotid artery atherosclerosis: a prospective cohort study.

OBJECTIVES: Epidemiological studies have demonstrated associations between long-term exposure to traffic-related air pollution and coronary heart disease (CHD). Atherosclerosis is the principal pathological process responsible for CHD events, but effects of traffic-related air pollution on progression of atherosclerosis are not clear. This study aimed to investigate associations between long-term exposure to traffic-related air pollution and progression of carotid artery atherosclerosis. SETTING: Healthy volunteers in metropolitan Vancouver, Canada. PARTICIPANTS AND OUTCOME MEASURES: 509 participants aged 30-65 years were recruited and followed for approximately 5 years. At baseline and end of follow-up, participants underwent carotid artery ultrasound examinations to assess atherosclerosis severity, including carotid intima-media thickness, plaque area, plaque number and total area. Annual change of each atherosclerosis marker during the follow-up period was calculated as the difference between these two measurements divided by years of follow-up. Living close to major roads was defined as ≤150 m from a highway or ≤50 m from a major road. Residential exposures to traffic-related air pollutants including black carbon, fine particles, nitrogen dioxide and nitric oxide were estimated using high-resolution land-use regression models. The data were analysed using general linear models adjusting for various covariates. RESULTS: At baseline, there were no significant differences in any atherosclerosis markers between participants living close to and those living away from major roads. After follow-up, the differences in annual changes of these markers between these two groups were small and not statistically significant. Also, no significant associations were observed with concentrations of traffic-related air pollutants including black carbon, fine particles, nitrogen dioxide and nitric oxide. CONCLUSIONS: This study did not find significant associations between traffic-related air pollution and progression of carotid artery atherosclerosis in a region with lower levels and smaller contrasts of ambient air pollution.

Associations of ambient air pollution with chronic obstructive pulmonary disease hospitalization and mortality.

RATIONALE: Ambient air pollution has been suggested as a risk factor for chronic obstructive pulmonary disease (COPD). However, there is a lack of longitudinal studies to support this assertion. OBJECTIVES: To investigate the associations of long-term exposure to elevated traffic-related air pollution and woodsmoke pollution with the risk of COPD hospitalization and mortality. METHODS: This population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents aged 45-85 years who resided in Metropolitan Vancouver, Canada, during the exposure period and did not have known COPD at baseline were included in this study (n = 467,994). Residential exposures to traffic-related air pollutants (black carbon, particulate matter <2.5 µm in aerodynamic diameter, nitrogen dioxide, and nitric oxide) and woodsmoke were estimated using land-use regression models and integrating changes in residences during the exposure period. COPD hospitalizations and deaths during the follow-up period were identified from provincial hospitalization and death registration databases. MEASUREMENTS AND MAIN RESULTS: An interquartile range elevation in black carbon concentrations (0.97 × 10(-5)/m, equivalent to 0.78 µg/m(3) elemental carbon) was associated with a 6% (95% confidence interval, 2-10%) increase in COPD hospitalizations and a 7% (0-13%) increase in COPD mortality after adjustment for covariates. Exposure to higher levels of woodsmoke pollution (tertile 3 vs. tertile 1) was associated with a 15% (2-29%) increase in COPD hospitalizations. There were positive exposure-response trends for these observed associations. CONCLUSIONS: Ambient air pollution, including traffic-related fine particulate pollution and woodsmoke pollution, is associated with an increased risk of COPD.

Association of long-term exposure to community noise and traffic-related air pollution with coronary heart disease mortality.

In metropolitan areas, road traffic is a major contributor to ambient air pollution and the dominant source of community noise. The authors investigated the independent and joint influences of community noise and traffic-related air pollution on risk of coronary heart disease (CHD) mortality in a population-based cohort study with a 5-year exposure period (January 1994-December 1998) and a 4-year follow-up period (January 1999-December 2002). Individuals who were 45-85 years of age and resided in metropolitan Vancouver, Canada, during the exposure period and did not have known CHD at baseline were included (n = 445,868). Individual exposures to community noise and traffic-related air pollutants, including black carbon, particulate matter less than or equal to 2.5 µm in aerodynamic diameter, nitrogen dioxide, and nitric oxide, were estimated at each person's residence using a noise prediction model and land-use regression models, respectively. CHD deaths were identified from the provincial death registration database. After adjustment for potential confounders, including traffic-related air pollutants or noise, elevations in noise and black carbon equal to the interquartile ranges were associated with 6% (95% confidence interval: 1, 11) and 4% (95% confidence interval: 1, 8) increases, respectively, in CHD mortality. Subjects in the highest noise decile had a 22% (95% confidence interval: 4, 43) increase in CHD mortality compared with persons in the lowest decile. These findings suggest that there are independent effects of traffic-related noise and air pollution on CHD mortality.

Modeling population exposure to community noise and air pollution in a large metropolitan area.

Epidemiologic studies have shown that both air pollution and community noise are associated with cardiovascular disease mortality. Because road traffic is a major contributor to these environmental pollutants in metropolitan areas, it is plausible that the observed associations may be confounded by coexistent pollutants. As part of a large population-based cohort study to address this concern, we used a noise prediction model to assess annual average community noise levels from transportation sources in metropolitan Vancouver, Canada. The modeled annual average noise level was 64 (inter quartile range 60-68) dB(A) for the region. This model was evaluated by comparing modeled annual daytime A-weighted equivalent continuous noise levels (L(day)) with measured 5-min daytime A-weighted equivalent continuous noise levels (L(eq,day,5 min)) at 103 selected roadside sites in the study region. On average, L(day) was 6.2 (95% CI, 6.0-7.9) dB(A) higher than, but highly correlated (r=0.62; 95% CI, 0.48-0.72) with, L(eq,day,5 min). These results suggest that our model-based noise exposure assessment could approximately reflect actual noise exposure in the study region. Overall, modeled noise levels were not strongly correlated with land use regression estimates of traffic-related air pollutants including black carbon, particulate matter with aerodynamic diameter ≤2.5 µm (PM(2.5)), NO(2) and NO; the highest correlation was with black carbon (r=0.48), whereas the lowest correlation was with PM(2.5) (r=0.18). There was no consistent effect of traffic proximity on the correlations between community noise levels and traffic-related air pollutant concentrations. These results, consistent with previous studies, suggest that it is possible to assess potential adverse cardiovascular effects from long-term exposures to community noise and traffic-related air pollution in prospective epidemiologic studies.

Exposure to occupational noise and cardiovascular disease in the United States: the National Health and Nutrition Examination Survey 1999-2004.

BACKGROUND: Chronic exposure to occupational noise may be associated with increased risk of coronary heart disease (CHD) and hypertension. However, findings are inconsistent and many previous studies are limited by small sample size and inappropriate control for potential confounders. We used a nationally representative US sample to examine associations of self-reported exposure to occupational noise with CHD and hypertension. METHODS: This cross-sectional study included 6307 participants of the National Health and Nutrition Examination Survey 1999-2004, aged ≥ 20 years and employed at the time of interview. Noise exposure assessment was based on self-reported exposure to loud noise in the workplace. RESULTS: Compared with never exposed participants, subjects chronically exposed to occupational noise had a 2-3-fold increased prevalence of angina pectoris, myocardial infarction, CHD and isolated diastolic hypertension. After adjustment for various covariates, the odds ratios (95% CIs) for angina pectoris, CHD and isolated diastolic hypertension were 2.91 (1.35 to 6.26), 2.04 (1.16 to 3.58) and 2.23 (1.21 to 4.12), respectively. There were clear exposure-response relationships for the observed associations. Associations of noise exposure with angina pectoris, myocardial infarction and CHD were particularly strong for participants aged < 50 years, men and current smokers. There was no significant increase in levels of cardiovascular biomarkers including blood lipids and circulating inflammatory mediators associated with noise exposure. CONCLUSIONS: Chronic exposure to occupational noise is strongly associated with prevalence of CHD, especially for young male current smokers. This study suggests that excess noise exposure in the workplace is an important occupational health issue and deserves special attention.

Long-term exposure to traffic-related air pollution and the risk of coronary heart disease hospitalization and mortality.

BACKGROUND: Epidemiologic studies have demonstrated that exposure to road traffic is associated with adverse cardiovascular outcomes. OBJECTIVES: We aimed to identify specific traffic-related air pollutants that are associated with the risk of coronary heart disease (CHD) morbidity and mortality to support evidence-based environmental policy making. METHODS: This population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents 45-85 years of age who resided in Metropolitan Vancouver during the exposure period and without known CHD at baseline were included in this study (n=452,735). Individual exposures to traffic-related air pollutants including black carbon, fine particles [aerodynamic diameter ≤ 2.5 µm (PM(2.5))], nitrogen dioxide (NO(2)), and nitric oxide were estimated at residences of the subjects using land-use regression models and integrating changes in residences during the exposure period. CHD hospitalizations and deaths during the follow-up period were identified from provincial hospitalization and death registration records. RESULTS: An interquartile range elevation in the average concentration of black carbon (0.94 × 10(-5)/m filter absorbance, equivalent to approximately 0.8 µg/m(3) elemental carbon) was associated with a 3% increase in CHD hospitalization (95% confidence interval, 1-5%) and a 6% increase in CHD mortality (3-9%) after adjusting for age, sex, preexisting comorbidity, neighborhood socioeconomic status, and copollutants (PM(2.5) and NO(2)). There were clear linear exposure-response relationships between black carbon and coronary events. CONCLUSIONS: Long-term exposure to traffic-related fine particulate air pollution, indicated by black carbon, may partly explain the observed associations between exposure to road traffic and adverse cardiovascular outcomes.

Changes in residential proximity to road traffic and the risk of death from coronary heart disease.

BACKGROUND: Residential proximity to road traffic is associated with increased coronary heart disease (CHD) morbidity and mortality. It is unknown, however, whether changes in residential proximity to traffic could alter the risk of CHD mortality. METHODS: We used a population-based cohort study with a 5-year exposure period and a 4-year follow-up period to explore the association between changes in residential proximity to road traffic and the risk of CHD mortality. The cohort comprised all residents aged 45-85 years who resided in metropolitan Vancouver during the exposure period and without known CHD at baseline (n = 450,283). Residential proximity to traffic was estimated using a geographic information system. CHD deaths during the follow-up period were identified using provincial death registration database. The data were analyzed using logistic regression. RESULTS: Compared with the subjects consistently living away from road traffic (>150 m from a highway or >50 m from a major road) during the 9-year study period, those consistently living close to traffic (

Sex-related differences in serum cotinine concentrations in daily cigarette smokers.

Self-reported use of cigarettes generally underestimates the true cigarette exposure of smokers. Serum cotinine is considered the best biomarker to evaluate tobacco exposure. This study determined whether or not there were any significant differences in serum cotinine concentrations between men and women when they reported smoking the same number of cigarettes per day. We analyzed cotinine and tobacco consumption data on 680 women and 840 men, aged 20 years or older, who smoked at least 100 cigarettes during their lifetime and were still actively smoking at the time of the National Health and Nutrition Examination Surveys (1999-2002). Overall, compared with men, women reported smoking fewer cigarettes per day (16.1 vs. 18.7, p<.001) and had lower serum cotinine concentrations (1163.3 nmol/L vs. 1343.9 nmol/L, p<.001). Women were more likely than men to smoke filtered (p = .018) and mentholated (p<.001) cigarettes. After adjustment for the number of cigarettes smoked per day, age, race, body mass index, poverty status, the use of either menthol or regular cigarettes, and the nicotine content in cigarettes, female compared with male smokers had lower serum cotinine concentrations (difference of 117.6 nmol/L; 95% CI = 42.6-192.6, p = .003). The difference was particularly notable in moderate to heavy smokers (i.e., those who smoked more than 15 cigarettes/day). These findings indicate that significant sex-related differences exist in serum cotinine levels among smokers, which suggests that self-reports may overestimate cigarette exposure in women compared with men.