Indoor air pollution and risk of lung cancer among Chinese female non-smokers

Purpose

To investigate indoor particulate matter (PM) level and various indoor air pollution exposure, and to examine their relationships with risk of lung cancer in an urban Chinese population, with a focus on non-smoking women.

Methods

We conducted a case–control study in Taiyuan, China, consisting of 399 lung cancer cases and 466 controls, of which 164 cases and 218 controls were female non-smokers. Indoor PM concentrations, including PM₁, PM_2.5, PM₇, PM₁₀, and TSP, were measured using a particle mass monitor. Unconditional logistic regression models were used to calculate odds ratios (ORs) and 95 % confidence intervals after adjusting for age, education, annual income, and smoking.

Results

Among non-smoking women, lung cancer was strongly associated with multiple sources of indoor air pollution 10 years ago, including heavy exposure to environmental tobacco smoke at work (aOR = 3.65), high frequency of cooking (aOR = 3.30), and solid fuel usage for cooking (aOR = 4.08) and heating (aOR_{coal stove} = 2.00). Housing characteristics related to poor ventilation, including single-story, less window area, no separate kitchen, no ventilator, and rarely having windows open, are associated with lung cancer. Indoor medium PM_2.5 concentration was 68 μg/m³, and PM₁₀ was 230 μg/m³. PM levels in winter are strongly correlated with solid fuel usage for cooking, heating, and ventilators. PM₁ levels in cases are more than 3 times higher than that in controls. Every 10 μg/m³ increase in PM₁ is associated with 45 % increased risk of lung cancer.

Conclusions

Indoor air pollution plays an important role in the development of lung cancer among non-smoking Chinese women.     

Breastfeeding and risk of ovarian cancer in two prospective cohorts

Objective To describe the association between breastfeeding and ovarian cancer risk in two prospective cohorts. Materials & methods We pooled data from the Nurses’ Health Study and Nurses’ Health Study II. There were 391 cases of epithelial ovarian cancer diagnosed among 149,693 parous women with up to 16 years of follow-up. Data were analyzed using multivariate Cox proportional hazards models, controlling for age, parity, duration of oral contraceptive use, tubal ligation, and age at menarche. Results Ever breastfeeding was associated with a non-significant reduction in ovarian cancer risk compared with never breastfeeding (RR = 0.86, 95% CI 0.70–1.06); the median duration of breastfeeding among women who breastfed was nine months. Breastfeeding of 18 or more months was associated with a significant decrease in ovarian cancer risk compared to never breastfeeding (RR = 0.66, 95% CI 0.46–0.96). For each month of breastfeeding the relative risk decreased by 2% (RR = 0.98 per month, 95% CI 0.97–1.00). Conclusions These data support a linear inverse association between breastfeeding and risk of epithelial ovarian cancer.     

Association between ambient air pollution and breast cancer risk: The multiethnic cohort study

Previous studies using different exposure methods to assess air pollution and breast cancer risk among primarily whites have been inconclusive. Air pollutant exposures of particulate matter and oxides of nitrogen were estimated by kriging (NO_x, NO₂, PM₁₀, PM_2.5), land use regression (LUR, NO_x, NO₂) and California Line Source Dispersion model (CALINE4, NO_x, PM_2.5) for 57,589 females from the Multiethnic Cohort, residing largely in Los Angeles County from recruitment (1993–1996) through 2010. Cox proportional hazards models were used to examine the associations between time-varying air pollution and breast cancer incidence adjusting for confounding factors. Stratified analyses were conducted by race/ethnicity and distance to major roads. Among all women, breast cancer risk was positively but not significantly associated with NO_x (per 50 parts per billion [ppb]) and NO₂ (per 20 ppb) determined by kriging and LUR and with PM_2.5 and PM₁₀ (per 10 μg/m³) determined by kriging. However, among women who lived within 500 m of major roads, significantly increased risks were observed with NO_x (hazard ratio [HR] = 1.35, 95% confidence interval [95% CI]: 1.02–1.79), NO₂ (HR = 1.44, 95% CI: 1.04–1.99), PM₁₀ (HR = 1.29, 95% CI: 1.07–1.55) and PM_2.5 (HR = 1.85, 95% CI: 1.15–2.99) determined by kriging and NO_x (HR = 1.21, 95% CI:1.01–1.45) and NO₂ (HR = 1.26, 95% CI: 1.00–1.59) determined by LUR. No overall associations were observed with exposures assessed by CALINE4. Subgroup analyses suggested stronger associations of NO_x and NO₂ among African Americans and Japanese Americans. Further studies of multiethnic populations to confirm the effects of air pollution, particularly near-roadway exposures, on the risk of breast cancer is warranted.     

Ambient air pollution and brain cancer mortality

Objective  

Growing evidence that ultrafine particles in ambient air can cause brain lesions in animals led us to investigate whether particulate components of air pollution may be associated with brain cancer risk in humans. Air pollution has been associated with respiratory disorders and cardiovascular morbidity and mortality, but associations between air pollutants and brain cancer have not been investigated in adults.     

Risk of cancer of the prostate and of the kidney parenchyma following bladder cancer

AIMS AND BACKGROUND: A registry-based cohort study of male patients with bladder cancer was conducted to determine the relative risk of second primary cancer of the prostate and kidney, the uni-/multivariate differences in relative risk according to patient characteristics, the cumulative risk by duration of the follow-up, and the prevalence:incidence ratio of prostate and kidney cancer cases detected in the first 6 months after the diagnosis of bladder cancer. METHODS: The complete case records of all male patients (n = 2025) diagnosed with bladder cancer between 1986 and 2002 were extracted from the database of the Romagna Cancer Registry: 1539 patients were eligible for analysis of the incidence of following prostate and kidney cancers, of the relative risk and the standardized incidence ratio specific for the time interval of follow-up. RESULTS: A total of 108 prostate cancer cases and 23 kidney cancer cases were observed during the follow-up. The relative risk of second primary cancer of the prostate and kidney was respectively 3.52 (95% CI, 2.89-4.25) and 3.90 (95% CI, 2.47-5.85). The absolute excess risk was 11.8 x 1000 for prostate cancer and 2.5 x 1000 for kidney cancer. The number of prevalent cases of prostate and kidney cancer detected was approximately 10 times greater than the expected number based on incidence rates from the general population. During the follow-up, incidence of prostate cancer stabilized at a level that was 3- to 4-fold greater than that expected. Despite fluctuations, a decrease was also observed for incidence of kidney cancer. CONCLUSIONS: In summary, our study showed the relatively constant high incidence of prostate and kidney cancers in bladder cancer patients over time. The possibility of subsequent cancer implies that an appropriate long surveillance is required. The pertinence depends on the duration of the follow-up as well as the degree of surveillance.     

Particulate matter air pollution and liver cancer survival

Particulate matter (PM) air pollution exposure has been associated with cancer incidence and mortality especially with lung cancer. The liver is another organ possibly affected by PM due to its role in detoxifying xenobiotics absorbed from PM. Various studies have investigated the mechanistic pathways between inhaled pollutants and liver damage, cancer incidence, and tumor progression. However, little is known about the effects of PM on liver cancer survival. Twenty thousand, two hundred and twenty‐one California Cancer Registry patients with hepatocellular carcinoma (HCC) diagnosed between 2000 and 2009 were used to examine the effect of exposure to ambient PM with diameter <2.5 μm (PM_2.5) on HCC survival. Cox proportional hazards models were used to estimate hazard ratios (HRs) relating PM_2.5 to all‐cause and liver cancer‐specific mortality linearly and nonlinearly—overall and stratified by stage at diagnosis (local, regional and distant)—adjusting for potential individual and geospatial confounders.PM_2.5 exposure after diagnosis was statistically significantly associated with HCC survival. After adjustment for potential confounders, the all‐cause mortality HR associated with a 1 standard deviation (5.0 µg/m³) increase in PM_2.5 was 1.18 (95% CI: 1.16–1.20); 1.31 (95% CI:1.26–1.35) for local stage, 1.19 (95% CI:1.14–1.23) for regional stage, and 1.05 (95% CI:1.01–1.10) for distant stage. These associations were nonlinear, with substantially larger HRs at higher exposures. The associations between liver cancer‐specific mortality and PM_2.5 were slightly attenuated compared to all‐cause mortality, but with the same patterns.Exposure to elevated PM_2.5 after the diagnosis of HCC may shorten survival, with larger effects at higher concentrations.     

Household air pollution and risk of incident lung cancer in urban China: A prospective cohort study

Household air pollution (HAP) is associated with the development of lung cancer, yet few studies investigated the exposure patterns and joint associations with tobacco smoking. In our study, we included 224 189 urban participants from China Kadoorie Biobank (CKB), 3288 of which diagnosed with lung cancer during the follow-up. Exposure to four HAP sources (solid fuels for cooking/heating/stove and environmental tobacco smoke exposure) was assessed at baseline. Distinct HAP patterns and their associations with lung cancer were examined through latent class analysis (LCA) and multivariable Cox regression. A total of 76.1% of the participants reported regular cooking and 52.2% reported winter heating, of which 9% and 24.7% used solid fuels, respectively. Solid fuel heating increased lung cancer risk (Hazards ratio [HR]: 1.25, 95% confidence interval [CI]: 1.08-1.46). LCA identified three HAP patterns; the “clean fuel cooking and solid fuel heating” pattern significantly increased lung cancer risk (HR: 1.25, 95% CI: 1.10-1.41), compared to low HAP pattern. An additive interaction was observed between heavy smoking and “clean fuel cooking and solid fuel heating” (relative excess risk [RERI]: 1.32, 95% CI: 0.29-2.47, attributable proportion [AP]: 0.23, 95% CI: 0.06-0.36). Cases resulting from solid fuel account for ~4% of total cases (population attribute fraction [PAF]_overall: 4.31%, 95% CI: 2.16%-6.47%, PAF_{ever smokers}: 4.38%, 95% CI: 1.54%-7.23%). Our results suggest that in urban China, solid fuel heating increased the risk of lung cancer, particularly among heavy smokers. The whole population could benefit from cleaner indoor air quality by reducing using solid fuels, especially smokers.     

Chronic long-term exposure to cadmium air pollution and breast cancer risk in the French E3N cohort

Cadmium, due to its estrogen-like activity, has been suspected to increase the risk of breast cancer; however, epidemiological studies have reported inconsistent findings. We conducted a case–control study (4,059 cases and 4,059 matched controls) nested within the E3N French cohort study to estimate the risk of breast cancer associated with long-term exposure to airborne cadmium pollution, and its effect according to molecular subtype of breast cancer (estrogen receptor negative/positive [ER−/ER+] and progesterone receptor negative/positive [PR−/PR+]). Atmospheric exposure to cadmium was assessed using a Geographic Information System-based metric, which included subject's residence-to-cadmium source distance, wind direction, exposure duration and stack height. Adjusted odds ratios (OR) and 95% confidence intervals (CI) were estimated using conditional logistic regression. Overall, there was no significant association between cumulative dose of airborne cadmium exposure and the risk of overall, premenopausal and postmenopausal breast cancer. However, by ER and PR status, inverse associations were observed for ER− (OR_{Q5 vs. Q1} = 0.63; 95% CI: 0.41–0.95, p_trend = 0.043) and for ER−/PR− breast tumors (OR_{Q4 vs. Q1} = 0.62; 95% CI: 0.40–0.95, OR_{Q5 vs. Q1} = 0.68; 95% CI: 0.42–1.07, p_trend = 0.088). Our study provides no evidence of an association between exposure to cadmium and risk of breast cancer overall but suggests that cadmium might be related to a decreased risk of ER− and ER−/PR− breast tumors. These observations and other possible effects linked to hormone receptor status warrant further investigations.     

Ambient air pollution and incident bladder cancer risk: Updated analysis of the Spanish Bladder Cancer Study

Although outdoor air pollution and particulate matter in outdoor air have been consistently linked with increased lung cancer risk, the evidence for associations at other cancer sites is limited. Bladder cancer shares several risk factors with lung cancer and some positive associations of ambient air pollution and bladder cancer risk have been observed. This study examined associations of ambient air pollution and bladder cancer risk in the large-scale Spanish Bladder Cancer Study. Estimates of ambient fine particulate matter (PM_2.5) and nitrogen dioxide (NO₂) concentrations were assigned to the geocoded participant residence of 938 incident bladder cancer cases and 973 hospital controls based on European multicity land-use regression models. Adjusted odds ratios (ORs) and 95% confidence intervals (CI) for associations of ambient air pollution and bladder cancer risk were estimated using unconditional logistic regression models. Overall, there was no clear association between either ambient PM_2.5 (OR per 5.9 μg/m³ = 1.06, 95% CI 0.71–1.60) or NO₂ (OR per 14.2 μg/m³ = 0.97, 95% CI 0.84–1.13) concentrations and incident bladder cancer risk. There was no clear evidence for effect modification according to age group, sex, region, education, cigarette smoking status, or pack-years. Results were also similar among more residentially stable participants and in two-pollutant models. Overall, there was no clear evidence for associations of ambient PM_2.5 and NO₂ concentrations and incident bladder cancer risk. Further research in other large-scale population studies is needed with detailed information on measured or modeled estimates of ambient air pollution concentrations and individual level risk factors.     

Lifestyle and cancer incidence and mortality risk depending on family history of cancer in two prospective cohorts

The extent to which a favorable lifestyle may lower cancer risk in subjects with a family history of cancer is unknown. We conducted a prospective study in two Swedish cohorts, the Malmö Diet and Cancer Study (MDCS; n = 25,604) and the Malmö Preventive Project (MPP; n = 16,216). The association between a favorable lifestyle (based on nonsmoking, normal weight, absence of excessive drinking, regular physical activity and healthy diet) and cancer incidence and mortality risk was assessed using Cox regression stratified by family history of cancer (all types). A favorable lifestyle was associated with a 22% (95% confidence interval [CI]: 18–26%) and 40% (95% CI: 36–44%) lower risk of cancer incidence and mortality, respectively, compared to an unfavorable lifestyle. No significant effect modification by family history was observed but there was a null association between lifestyle and cancer incidence among subjects with two or more affected first-degree relatives. The observed relative risk estimates comparing an unfavorable with a favorable lifestyle corresponded to standardized 10-year cancer incidence rates of 11.2 vs. 9.5% in the MDCS, and 4.4 vs. 3.2% in the MPP, and a reduction in 20-year cancer mortality rate from 11.7% to 7.4% in the MDCS and 6.7% to 3.9% in the MPP. Improved adherence to cancer prevention recommendations may reduce cancer incidence and mortality risk in the general population, however, further studies are needed to assess the impact of lifestyle on cancer incidence among subjects with strong familial or polygenic risk for specific cancers.     

Traffic‐related air pollution and risk for leukaemia of an adult population

Air pollution causes lung cancer, but associations with other cancers have not been established. We investigated whether long‐term exposure to traffic‐related air pollution is associated with the risk of the general population for leukaemia. We identified 1,967 people in whom leukaemia was diagnosed in 1992–2010 from a nation‐wide cancer registry and selected 3,381 control people at random, matched on sex and year of birth, from the entire Danish population. Residential addresses since 1971 were traced in a population registry, and outdoor concentrations of NO_x and NO₂, as indicators of traffic‐related air pollution, were calculated at each address in a dispersion model. We used conditional logistic regression to estimate the risk for leukaemia after adjustment for income, educational level, cohabitation status and co‐morbidity. In linear analyses, we found odds ratios for acute myeloid leukaemia of 1.20 (95% confidence interval: 1.04–1.38) per 20 µg/m³ increase in NO_x and 1.31 (1.02–1.68) per 10 µg/m³ increase in NO₂, calculated as time‐weighted average exposure at all addresses since 1971. We found no association with chronic myeloid or lymphocytic leukaemia. This study indicates an association between long‐term exposure to traffic‐related air pollution and acute myeloid leukaemia in the general population, but not for other subtypes of leukaemia.     

Sugar-sweetened soft drink consumption and risk of pancreatic cancer in two prospective cohorts.

BACKGROUND: A history of diabetes mellitus and a diet high in glycemic load are both potential risk factors for pancreatic cancer. Sugar-sweetened soft drinks are a prevalent source of readily absorbable sugars and have been associated with an increased risk of obesity and diabetes. We investigated whether higher consumption of sugar-sweetened soft drinks increases the risk of pancreatic cancer. METHODS: We examined the relation between consumption of sugar-sweetened soft drinks and the development of pancreatic cancer in the Nurses' Health Study and the Health Professionals Follow-up Study. Among 88,794 women and 49,364 men without cancer at baseline, we documented 379 cases of pancreatic cancer during up to 20 years of follow-up. Soft drink consumption was first assessed at baseline (1980 for the women, 1986 for the men) and updated periodically thereafter. RESULTS: Compared with participants who largely abstained from sugar-sweetened soft drinks, those who consumed more than three sugar-sweetened soft drinks weekly experienced overall a multivariate relative risk (RR) of pancreatic cancer of 1.13 [95% confidence interval (95% CI), 0.81-1.58; P for trend = 0.47]. Women in the highest category of sugar-sweetened soft drink intake did experience a significant increase in risk (RR, 1.57; 95% CI, 1.02-2.41; P for trend = 0.05), whereas there was no association between sweetened soft drink intake and pancreatic cancer among men. Among women, the risk associated with higher sugar-sweetened soft drink was limited to those with elevated body mass index (>25 kg/m(2); RR, 1.89; 95% CI, 0.96-3.72) or with low physical activity (RR, 2.02; 95% CI, 1.06-3.85). In contrast, consumption of diet soft drinks was not associated with an elevated pancreatic cancer risk in either cohort. CONCLUSION: Although soft drink consumption did not influence pancreatic cancer risk among men, consumption of sugar-sweetened soft drinks may be associated with a modest but significant increase in risk among women who have an underlying degree of insulin resistance.     

小环境污染、精神因素与肺癌的关系

目的探讨室内环境污染、神经精神等因素与肺癌发生的关系.方法利用1:3配对的病例对照研究调查被访问者既往暴露史,用条件Logistic回归分析诸因素的比值比及其95%可信区间.结果经调整混杂因素后本研究结果提示,用煤量≥46kg/m2可使肺癌危险性增加2.22倍,煤炉取暖增加肺癌危险性2.13倍;婚姻生活不和谐或破裂、自我调节能力差、不易适应环境以及人际关系较差均使肺癌危险性增加5倍以上.经常暴露于室内油烟,且精神长期处于压抑状态或具有较大的精神创伤,可使肺癌危险性明显增加.结论内空气污染、神经精神因素等是肺癌发生的重要因素.