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 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.     

Long‐term exposure to fine particulate matter air pollution and the risk of lung cancer among participants of the Canadian National Breast Screening Study

Recently, air pollution has been classified as a carcinogen largely on the evidence of epidemiological studies of lung cancer. However, there have been few prospective studies that have evaluated associations between fine particulate matter (PM_2.5) and cancer at lower concentrations. We conducted a prospective analysis of 89,234 women enrolled in the Canadian National Breast Screening Study between 1980 and 1985, and for whom residential measures of PM_2.5 could be assigned. The cohort was linked to the Canadian Cancer Registry to identify incident lung cancers through 2004. Surface PM_2.5 concentrations were estimated using satellite data. Cox proportional hazards models were used to characterize associations between PM_2.5 and lung cancer. Hazard ratios (HRs) and 95% confidence intervals (CIs) computed from these models were adjusted for several individual‐level characteristics, including smoking. The cohort was composed predominantly of Canadian‐born (82%), married (80%) women with a median PM_2.5 exposure of 9.1 µg/m³. In total, 932 participants developed lung cancer. In fully adjusted models, a 10 µg/m³ increase in PM_2.5 was associated with an elevated risk of lung cancer (HR: 1.34; 95% CI = 1.10, 1.65). The strongest associations were observed with small cell carcinoma (HR: 1.53; 95% CI = 0.93, 2.53) and adenocarcinoma (HR: 1.44; 95% CI = 1.06, 1.97). Stratified analyses suggested increased PM_2.5 risks were limited to those who smoked cigarettes. Our findings are consistent with previous epidemiological investigations of long‐term exposure to PM_2.5 and lung cancer. Importantly, they suggest associations persist at lower concentrations such as those currently found in Canadian cities.     

Air pollution and incidence of cancers of the stomach and the upper aerodigestive tract in the European Study of Cohorts for Air Pollution Effects (ESCAPE)

Air pollution has been classified as carcinogenic to humans. However, to date little is known about the relevance for cancers of the stomach and upper aerodigestive tract (UADT). We investigated the association of long‐term exposure to ambient air pollution with incidence of gastric and UADT cancer in 11 European cohorts. Air pollution exposure was assigned by land‐use regression models for particulate matter (PM) below 10 µm (PM₁₀), below 2.5 µm (PM_2.5), between 2.5 and 10 µm (PM_coarse), PM_2.5 absorbance and nitrogen oxides (NO₂ and NO_X) as well as approximated by traffic indicators. Cox regression models with adjustment for potential confounders were used for cohort‐specific analyses. Combined estimates were determined with random effects meta‐analyses. During average follow‐up of 14.1 years of 305,551 individuals, 744 incident cases of gastric cancer and 933 of UADT cancer occurred. The hazard ratio for an increase of 5 µg/m³ of PM_2.5 was 1.38 (95% CI 0.99; 1.92) for gastric and 1.05 (95% CI 0.62; 1.77) for UADT cancers. No associations were found for any of the other exposures considered. Adjustment for additional confounders and restriction to study participants with stable addresses did not influence markedly the effect estimate for PM_2.5 and gastric cancer. Higher estimated risks of gastric cancer associated with PM_2.5 was found in men (HR 1.98 [1.30; 3.01]) as compared to women (HR 0.85 [0.5; 1.45]). This large multicentre cohort study shows an association between long‐term exposure to PM_2.5 and gastric cancer, but not UADT cancers, suggesting that air pollution may contribute to gastric cancer risk.     

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.     

Outdoor air pollution and risk for kidney parenchyma cancer in 14 European cohorts

Several studies have indicated weakly increased risk for kidney cancer among occupational groups exposed to gasoline vapors, engine exhaust, polycyclic aromatic hydrocarbons and other air pollutants, although not consistently. It was the aim to investigate possible associations between outdoor air pollution at the residence and the incidence of kidney parenchyma cancer in the general population. We used data from 14 European cohorts from the ESCAPE study. We geocoded and assessed air pollution concentrations at baseline addresses by land‐use regression models for particulate matter (PM₁₀, PM_2.5, PM_coarse, PM_2.5 absorbance (soot)) and nitrogen oxides (NO₂, NO_x ), and collected data on traffic. We used Cox regression models with adjustment for potential confounders for cohort‐specific analyses and random effects models for meta‐analyses to calculate summary hazard ratios (HRs). The 289,002 cohort members contributed 4,111,908 person‐years at risk. During follow‐up (mean 14.2 years) 697 incident cancers of the kidney parenchyma were diagnosed. The meta‐analyses showed higher HRs in association with higher PM concentration, e.g. HR = 1.57 (95%CI: 0.81–3.01) per 5 μg/m³ PM_2.5 and HR = 1.36 (95%CI: 0.84–2.19) per 10^?5m^?1 PM_2.5 absorbance, albeit never statistically significant. The HRs in association with nitrogen oxides and traffic density on the nearest street were slightly above one. Sensitivity analyses among participants who did not change residence during follow‐up showed stronger associations, but none were statistically significant. Our study provides suggestive evidence that exposure to outdoor PM at the residence may be associated with higher risk for kidney parenchyma cancer; the results should be interpreted cautiously as associations may be due to chance.     

Potential causal links of long-term air pollution with lung cancer incidence: From the perspectives of mortality and hospital admission in a large cohort study in southern China

Evidence on the potential causal links of long-term air pollution exposure with lung cancer incidence (reflected by mortality and hospital admission) was limited, especially based on large cohorts. We examined the relationship between lung cancer and long-term exposure to particulate matter (PM, including PM_2.5, PM₁₀ and PM_10-2.5) and nitrogen dioxide (NO₂) among a large cohort of general Chinese adults using causal inference approaches. The study included 575 592 participants who were followed up for an average of 8.2 years. The yearly exposure of PM and NO₂ was estimated through satellite-based random forest approaches and the ordinary kriging method, respectively. Marginal structural Cox models were used to examine hazard ratios (HRs) of mortality and hospital admission due to lung cancer following air pollution exposure, adjusting for potential confounders. The HRs of mortality due to lung cancer were 1.042 (95% confidence interval [CI]: 1.033-1.052), 1.032 (95% CI:1.024-1.041) and 1.052 (95% CI:1.041-1.063) for each 1 μg/m³ increase in PM_2.5, PM₁₀ and NO₂, respectively. In addition, we observed statistically significant effects of PMs on hospital admission due to lung cancer. The HRs (95%CI) were 1.110 (1.027-1.201), 1.067 (1.020-1.115) and 1.079 (1.010-1.153) for every 1 μg/m³ increase in PM_2.5, PM₁₀, PM_10-2.5, respectively. Furthermore, we found larger effect estimates among the elderly and those who exercised more frequently. We provided the most comprehensive evidence of the potential causal links between two outcomes of lung cancer and long-term air pollution exposure. Relevant policies should be developed, with special attention to protecting the vulnerable groups of the population.     

The effect of atmospheric particulate matter on survival of breast cancer among US females

Short-term effects of ambient particulate matter (PM) on cardiopulmonary morbidity and mortality have been consistently documented. However, no study has investigated its long-term effects on breast cancer survival. We selected all female breast cancer cases (n = 255,128) available in the California Surveillance Epidemiology and End Results cancer data. These cases were linked to 1999–2009 California county-level PM daily monitoring data. We examined the effect of PM on breast cancer survival. Results from Kaplan–Meier survival analysis show that female breast cancer cases living in areas with higher levels of PM₁₀ and PM_2.5 had a significant shorter survival than those living in areas with lower exposures (p < 0.0001). The results from marginal cox proportional hazards models suggest that exposure to higher PM₁₀ (HR 1.13, 95 % CI 1.02–1.25, per 10 μg/m³) or PM_2.5 (HR 1.86, 95 % CI 1.12–3.10, per 5 μg/m³) was significantly associated with early mortality among female breast cancer cases after adjusting for individual-level covariates such as demographic factors, cancer stage and year diagnosed, and county-level covariates such as socioeconomic status and accessibility to medical resources. Interactions between cancer stage and PM were also observed; the effect of PM on survival was more pronounced among individuals diagnosed with early stage cancers. This study suggests that exposure to high levels of PM may have deleterious effects on the length of survival from breast cancer, particularly among women diagnosed with early stage cancers. The findings from this study warrant further investigation.     

Serum total thiol levels and the risk of lung,colorectal, breast and prostate cancer: A prospective case–cohort study

Free thiol groups of intra and extracellular molecules are considered to be antioxidative and to protect cells from damage caused by free radicals. However, the associations of serum total thiol levels (TTL) with the incidences of the four most frequent cancer sites have not yet been investigated in a large population-based, prospective study. TTL was measured in case–cohort design in a sample from the population-based, Norwegian Tromsø 3 study (cancer cases: n = 941; random subcohort: n = 1,000) and was repeatedly measured at Tromsø 5. Hazard ratios (HRs) and 95% confidence intervals (95% CIs) were estimated by weighted multivariable-adjusted Cox regression with time-dependent modeling of TTL for incident lung, colorectal, breast and prostate cancer. High serum TTL were associated with a reduced risk of all four major cancers. The associations with lung (top vs. bottom tertile: HR, 0.64; 95% CI, 0.41, 0.99) and breast cancer (top vs. bottom tertile: HR, 0.64; 95% CI, 0.42, 0.96) were statistically significant, whereas associations with colorectal (top vs. bottom tertile: HR, 0.79; 95% CI, 0.54, 1.16) and prostate cancer (top vs. bottom tertile: HR, 0.79; 95% CI, 0.53, 1.17) were not statistically significant but pointed in the same protective direction. These findings from a large, prospective Norwegian cohort study suggest a preventive role of thiols against the development of the four most frequent cancers. Whereas associations with breast and lung cancer could be shown with statistical significance, larger studies are needed to corroborate potential associations of TTL with colorectal and prostate cancer.     

High-Ambient Air Pollution Exposure Among Never Smokers Versus Ever Smokers With Lung Cancer

IntroductionAir pollution may play an important role in the development of lung cancer in people who have never smoked, especially among East Asian women. The aim of this study was to compare cumulative ambient air pollution exposure between ever and never smokers with lung cancer.MethodsA consecutive case series of never and ever smokers with newly diagnosed lung cancer were compared regarding their sex, race, and outdoor and household air pollution exposure. Using individual residential history, cumulative exposure to outdoor particulate matter (PM_2.5) in a period of 20 years was quantified with a high-spatial resolution global exposure model.ResultsOf the 1005 patients with lung cancer, 56% were females and 33% were never smokers. Compared with ever smokers with lung cancer, never smokers with lung cancer were significantly younger, more frequently Asian, less likely to have chronic obstructive pulmonary disease or a family history of lung cancer, and had higher exposure to outdoor PM_2.5 but lower exposure to secondhand smoke. Multivariable logistic regression analysis revealed a significant association with never-smoking patients with lung cancer and being female (OR = 4.01, 95% confidence interval [CI]: 2.76–5.82, p < 0.001), being Asian (OR_{Asian versus non-Asian} = 6.48, 95% CI: 4.42–9.50, p < 0.001), and having greater exposure to air pollution (OR_{ln_PM2.5} = 1.79, 95% CI: 1.10–7.2.90, p = 0.019).ConclusionsCompared with ever-smoking patients with lung cancer, never-smoking patients had strong associations with being female, being Asian, and having air pollution exposures. Our results suggest that incorporation of cumulative exposure to ambient air pollutants be considered when assessing lung cancer risk in combination with traditional risk factors.     

Alcohol consumption and risk of breast cancer by molecular subtype: Prospective analysis of the nurses' health study after 26 years of follow‐up

Alcohol consumption is a consistent risk factor for breast cancer, although it is unclear whether the association varies by breast cancer molecular subtype. We investigated associations between cumulative average alcohol intake and risk of breast cancer by molecular subtype among 105,972 women in the prospective Nurses' Health Study cohort, followed from 1980 to 2006. Breast cancer molecular subtypes were defined according to estrogen receptor (ER), progesterone receptor, human epidermal growth factor 2 (HER2), cytokeratin 5/6, and epidermal growth factor status from immunostained tumor microarrays in combination with histologic grade. Multivariable Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI). Competing risk analyses were used to assess heterogeneity by subtype. We observed suggestive heterogeneity in associations between alcohol and breast cancer by subtype (p_het = 0.06). Alcohol consumers had an increased risk of luminal A breast cancers [n = 1,628 cases, per 10 g/day increment HR (95%CI) = 1.10(1.05–1.15)], and an increased risk that was suggestively stronger for HER2‐type breast cancer [n = 160 cases, HR (95%CI) = 1.16(1.02–1.33)]. We did not observe statistically significant associations between alcohol and risk of luminal B [n = 631 cases, HR (95%CI) = 1.08(0.99–1.16)], basal‐like [n = 254 cases, HR (95%CI) = 0.90(0.77–1.04)], or unclassified [n = 87 cases, HR (95%CI) = 0.90(0.71–1.14)] breast cancer. Alcohol consumption was associated with increased risk of luminal A and HER2‐type breast cancer, but not significantly associated with other subtypes. Given that ERs are expressed in luminal A but not in HER2‐type tumors, our findings suggest that other mechanisms may play a role in the association between alcohol and breast cancer.     

Association between meat consumption and risk of breast cancer: Findings from the Sister Study

Meat consumption has been postulated to increase the risk of breast cancer, but this association has not been consistently seen. We examined the association between consumption of different types of meat, meat mutagens and incident invasive breast cancer. Information on consumption of different meat categories and meat cooking practice behaviors was obtained from 42,012 Sister Study participants who completed a Block 1998 Food Frequency Questionnaire at enrollment (2003–2009) and satisfied eligibility criteria. Exposure to meat type and meat mutagens was calculated, and associations with invasive breast cancer risk were estimated using multivariable Cox proportional hazards regression. During follow-up (mean, 7.6 years), 1,536 invasive breast cancers were diagnosed at least 1 year after enrollment. Increasing consumption of red meat was associated with increased risk of invasive breast cancer (HR_{highest vs. lowest quartile}:1.23, 95% CI: 1.02–1.48, p_trend = 0.01). Conversely, increasing consumption of poultry was associated with decreased invasive breast cancer risk (HR _{highest vs. lowest quartile}: 0.85; 95% CI: 0.72–1.00; p_trend = 0.03). In a substitution model with combined red meat and poultry consumption held constant, substituting poultry for red meat was associated with decreased invasive breast cancer risk (HR _{highest vs. lowest quartile} of poultry consumption: 0.72, 95% CI: 0.58–0.89). No associations were observed for cooking practices, estimated heterocyclic amines or heme iron from red meat consumption with breast cancer risk. Red meat consumption may increase the risk of invasive breast cancer, whereas poultry consumption may be associated with reduced risk. Substituting poultry for red meat could reduce breast cancer risk.     

Long-term exposure to air pollution and risk of non-Hodgkin lymphoma in Denmark: A population-based case–control study

There is limited evidence regarding a possible association between exposure to ambient air pollutants and the risk of non-Hodgkin lymphoma (NHL). Previous epidemiological studies have relied on crude estimations for air pollution exposure and/or small numbers of NHL cases. The objective of our study was to analyze this association based on air pollution modeled at the address level and NHL cases identified from the nationwide Danish Cancer Registry. We identified 20,874 incident NHL cases diagnosed between 1989 and 2014 and randomly selected 41,749 controls matched on age and gender among the entire Danish population. We used conditional logistic regression to estimate odds ratios (ORs) and adjusted for individual and neighborhood level sociodemographic variables. There was no association between exposure to PM_2.5, BC, O₃, SO₂ or NO₂ and overall risk of NHL but several air pollutants were associated with higher risk of follicular lymphoma, but statistically insignificant, for example, PM_2.5 (OR = 1.15 per 5 μg/m³; 95% CI: 0.98–1.34) and lower risk for diffuse large B-cell lymphoma (OR = 0.92 per 5 μg/m³; 95% CI: 0.82–1.03). In this population-based study, we did not observe any convincing evidence of a higher overall risk for NHL with higher exposure to ambient air pollutants.     

Association between ambient exposure to PM2.5 and upper aerodigestive tract cancer in Los Angeles

Fine particulate matter (PM_2.5) contains carcinogens similar to those generated by tobacco smoking, which may increase the risks of developing smoking-related cancers, such as upper aerodigestive track (UADT) cancers, for both smokers and never-smokers. Therefore, it is imperative to understand the relation between ambient PM_2.5 exposure and risk of UADT cancers. A population-based case–control study involving 565 incident UADT cancer cases and 983 controls was conducted in Los Angeles County from 1999 to 2004. The average residential PM_2.5 concentration 1 year before the diagnosis date for cases and the reference date for controls was assessed using a chemical transport model. The association between ambient PM_2.5 and the UADT cancers was estimated by unconditional logistic regression, adjusting for confounders at the individual and block-group level. Stratified analyses were conducted by sex, tobacco smoking status and UADT subsites. We also assessed the interaction between PM_2.5 and tobacco smoking on UADT cancers. PM_2.5 concentrations were associated with an elevated odds of UADT cancers (adjusted odds ratio = 1.21 per interquartile range [4.5 μg/m³] increase; 95% confidence interval: 1.02, 1.44). The association between PM_2.5 and UADT cancers was similar across UADT subsites, sex and tobacco smoking status. The interaction between PM_2.5 and tobacco smoking on UADT cancers was approximately additive on the odds scale. The effect estimate for PM_2.5 and UADT cancers was similar among never smokers. Our findings support the hypothesis that exposure to PM_2.5 increases the risk of UADT cancers. Improvements in air quality may reduce the risk of UADT cancers.     

Fruit and vegetable consumption and breast cancer incidence: Repeated measures over 30 years of follow-up

We evaluated the relation of fruit and vegetable consumption, including specific fruits and vegetables, with incident breast cancer characterized by menopausal status, hormone receptor status and molecular subtypes. Fruit and vegetable consumption, cumulatively averaged across repeated, validated questionnaires, was examined in relation to risk of invasive breast cancer among 182,145 women initially aged 27–59 years in the Nurses’ Health Study (NHS, 1980–2012) and NHSII (1991–2013). Cox proportional hazards regression, adjusted for known risk factors, was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) and assessed tumors by hormone receptor status and molecular subtypes. We prospectively documented 10,911 invasive breast cancer cases. Greater intake of total fruits and vegetables, especially cruciferous and yellow/orange vegetables, was associated with significantly lower breast cancer risk (>5.5 vs. ≤2.5 servings/day HR = 0.89, 95% CI = 0.83–0.96; p_trend = 0.006). Intake of total vegetables was especially associated with lower risk of estrogen receptor negative tumors (HR per 2 additional servings/day as a continuous variable = 0.84, 95%CI = 0.77–0.93; p_{heterogeneity} = 0.02). Among molecular subtypes, higher intake of total fruits and vegetables (HR per 2 additional servings/day as a continuous variable) was most strongly associated with lower risk of human epidermal growth factor receptor 2 (HER2)-enriched (HR = 0.79, 95%CI = 0.67–0.93), basal-like (HR = 0.84, 95%CI = 0.72–0.97) and luminal A (HR = 0.94, 95%CI = 0.89–0.99), but not with luminal B tumors (p_{heterogeneity} = 0.03). In conclusion, our findings support that higher intake of fruits and vegetables, and specifically cruciferous and yellow/orange vegetables, may reduce the risk of breast cancer, especially those that are more likely to be aggressive tumors.     

Supplemental one-carbon metabolism related B vitamins and lung cancer risk in the Women's Health Initiative

We and others have reported associations between B vitamins principally involved in one-carbon metabolism and increased lung cancer risk; however, results for women have been inconsistent. Here we report on the association of supplemental vitamins B₆, folic acid and B₁₂ intake and lung cancer risk using data from the Women's Health Initiative (WHI) study of postmenopausal women. Between 1993 and 1998, 161,808 women were recruited to participate in the WHI at 40 clinical centers in the US. After exclusions, 159,232 women were available for analysis and followed prospectively for an average of 18.3 years. Among them, 3,836 incident lung cancer cases were diagnosed. At baseline, supplemental B vitamins from multivitamins, vitamin mixtures and individual supplements were assessed. Adjusted Cox regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for associations between supplemental B vitamin intake and lung cancer risk. Relative to no intake, women who took ≥50 mg/day of vitamin B₆ had 16% (HR 0.84, 95% CI: 0.71–0.99) reduced lung cancer risk. Associations did not differ significantly by smoking status or lung cancer histology. Intakes of folic acid and vitamin B₁₂ were not associated with risk. There is a need for replication of our findings from other large, prospective studies with similar high-quality measurement of supplement intakes before any recommendations can be made at present on B₆ supplementation for lung cancer prevention in women.     

Chronic inflammation and risk of lung cancer in older adults in the health,aging and body composition cohort study

Objectives

We examined the association between three inflammatory markers (Interleukin (IL)-6, C-reactive protein (CRP), tumor necrosis factor (TNF)-α) and incident lung cancer using baseline, updated, and averaged inflammatory measures in older adults.

Observational and genetic plasma YKL‐40 and cancer in 96,099 individuals from the general population

Plasma YKL‐40 is high in patients with cancer and in individuals who later develop cancer. Whether YKL‐40 is only a marker or indeed a cause of cancer is presently unknown. We tested the hypothesis that observationally and genetically, high plasma YKL‐40 is associated with high risk of cancer. For this purpose, we performed cohort and Mendelian randomization studies in 96,099 individuals from the Danish general population. Plasma levels of YKL‐40 were measured in 21,643 and CHI3L1 rs4950928 was genotyped in 94,568 individuals. From 1943 through 2011, 2,291 individuals developed gastrointestinal cancer, 913 developed lung cancer, 2,863 women developed breast cancer, 1,557 men developed prostate cancer and 5,146 individuals developed other cancer. Follow‐up was 100% complete. Multifactorially and CRP adjusted hazard ratio (HR) for gastrointestinal cancer was 1.82 (95%CI, 1.16–2.86) for 96–100% versus 0–33% YKL‐40 percentile category. Corresponding HR were 1.71 (0.95–3.07) for lung cancer, but insignificant for breast cancer, prostate cancer and other cancers. CHI3L1 rs4950928 genotype was associated with plasmaYKL‐40 levels, but not with risk of any cancer category. For gastrointestinal cancer, a doubling in YKL‐40 was associated with a multifactorially and CRP adjusted observational HR of 1.14(1.05–1.23) for gastrointestinal cancer, but a corresponding genetic odds ratio of 1.06(0.94–1.18). For lung cancer, corresponding risk estimates were 1.11(1.00–1.22) observationally and 1.01(0.84–1.20) genetically. For other cancer categories, observational and genetic findings were insignificant. This study shows that high plasma YKL‐40 levels were associated with high risk of gastrointestinal and likely of lung cancer, but genetic high levels were not.     

Associations of metabolic syndrome and C‐reactive protein with mortality from total cancer,obesity‐linked cancers and breast cancer among women in NHANES III

Although metabolic syndrome (MetS) is a prognostic factor for cancer occurrence, the association of MetS and cancer mortality remains unclear. The purpose of this study was to evaluate whether MetS, components of MetS and C‐reactive protein (CRP) are associated with cancer mortality in women. A total of 400 cancer deaths, with 140 deaths from obesity‐linked‐cancers (OLCas), [breast (BCa), colorectal, pancreatic and endometrial], linked through the National Death Index, were identified from 10,104 eligible subjects aged ≥18 years. Cox proportional hazards regression was used to estimate multivariable‐adjusted hazard ratios (HR) for cancer mortality. MetS was associated with increased deaths for total cancer [HR = 1.33, 95% confidence interval (CI) 1.04–1.70] and BCa [HR = 2.1, 95% CI, 1.09–4.11]. The risk of total cancer [HR = 1.7, 95% CI, 1.12–2.68], OLCas [HR = 2.1, 95% CI, 1.00–4.37] and BCa [HR = 3.8, 95% CI, 1.34–10.91] mortality was highest for women with all MetS components abnormal, compared to those without MetS. Linear associations of blood‐pressure [HR = 2.5, 1.02–6.12, Quartile (Q) 4 vs Q1, p trend = 0.004] and blood‐glucose [HR = 2.2, 1.04–4.60, Q4 vs. Q1, p trend = 0.04] with total‐OLCas mortality were observed. A threefold increased risk of BCa mortality was observed for women with enlarged waist circumference, ≥100.9 cm, [HR = 3.5, 1.14–10.51, p trend = 0.008] and in those with increased blood glucose, ≥101 mg/dL, [HR = 3.2, 1.11–9.20, p trend = 0.03] compared to those in Q1. None of the components of MetS were associated with total‐cancer mortality. CRP was not associated with cancer mortality. In conclusion, MetS is associated with total‐cancer and breast‐cancer mortality, with waist circumference, blood pressure and blood glucose as independent predictors of OLCas and BCa mortality.     

Blood arsenic levels and the risk of familial breast cancer in Poland

Arsenic is recognized as a potent carcinogen at high concentrations, but the relationship between environmental arsenic and breast cancer risk has not well been studied. Most research has focused on the effect of arsenic in populations with high endemic exposure, and not in populations with arsenic levels within normal limits. We sought to determine if blood arsenic levels predict the risk of breast and other cancers risk among women in northern Poland. The cohort consisted of 1,702 healthy women, aged 40 and above, identified between 2010 and 2017. Blood arsenic level was determined by inductively coupled plasma mass spectrometry. After an average of 4.5 years of follow-up (range 0.7–7.3 years), there were 110 incident cases of cancer diagnosed in the cohort, including 68 cases of breast cancer. Women in the highest quartile of arsenic had a highly significant 13-fold increased risk of developing breast cancer, compared to women in the lowest quartile (hazard ratio [HR] = 13.2; 95% confidence interval [CI] 4.02–43.0). Results were similar for arsenic and all incident cancers (HR quartile 4 vs. quartile 1 = 13.3; 95% CI 4.78–37.0). If confirmed, our study suggests that the blood arsenic level may be a useful predictive marker of cancer risk in women.