The IARC Perspective on Colorectal Cancer Screening

Colorectal cancer, which is the third most common cancer in men and the second most common in women, represents almost 10% of the annual global cancer incidence. Incidence rates of colorectal cancer show a strong positive gradient with an increasing level of economic development. Even so, the net 5-year rate of survival decreases with lower levels of income, with rates reaching 60% in high-income countries but falling to 30% or less in low-income countries. Established risk factors for colorectal cancer include consumption of processed meats, consumption of alcoholic beverages, tobacco smoking, and excess body fat, whereas consumption of dietary fiber and dairy products and increased levels of physical activity decrease the risk. In addition, certain subgroups of the population are at increased risk owing to genetic predisposition (e.g., the Lynch syndrome), a family or personal history of colorectal neoplasia, or medical conditions (e.g., inflammatory bowel disease) that have been associated with colorectal cancer

The effect of occupational exposure to welding fumes on trachea, bronchus and lung cancer: A protocol for a systematic review and meta-analysis from the WHO/ILO Joint Estimates of the Work-related Burden of Disease and Injury

The World Health Organization (WHO) and the International Labour Organization (ILO) are developing joint estimates of the work-related burden of disease and injury (WHO/ILO Joint Estimates), with contributions from a large network of experts. Welding fumes have been classified as carcinogenic to humans (Group 1) by the International Agency for Research on Cancer (IARC); this assessment found sufficient evidence from studies in humans that welding fumes are a cause of lung cancer. In this article, we present the protocol for a systematic review of parameters for estimating the number of deaths and disability-adjusted life years from trachea, bronchus and lung cancer attributable to occupational exposure to welding fumes, to inform the development of the WHO/ILO Joint Estimates

The role of coffee consumption in breast and ovarian cancer risk: updated meta-analyses

Background: Coffee consumption in relation to female hormone-related cancers has been investigated but metaanalyses regarding breast and ovarian cancer include studies published up to 2012 with inconsistent results for ovarian cancer. Methods: We conducted two updated meta-analyses of studies published up to June 2016 to quantify the association of coffee intake with breast and ovarian cancer risk with random effects models. We used the dataset developed by the International Agency for Research on Cancer Working Group for Monograph 116 meeting (May 2016). We additionally performed a PubMed search in June 2016. Results: Summary relative risks (RRs) (95% confidence intervals (CI)) for the study-specific highest vs. lowest coffee consumption were for breast and ovarian cancer respectively: 0.97 (0.93–1.00, Ι2 5.5%, 40 studies, 76,728 cases) and 1.03 (0.93–1.14, Ι 2 31.9%, 31 studies, 13,111 cases). For decaffeinated coffee the corresponding RRs were: 1.00 (0.93-1.08, I2 32.2%, 13 studies) and 0.83 (0.71-0.96, I2 about 0%, 9 studies). The association of coffee with ovarian cancer risk was higher among publications before (RR=1.37, 1.12–1.69) compared to after 2000 (RR=0.96, 0.86-1.06). Conclusion: Our meta-analyses provide strong, quantitative evidence that coffee consumption is not related to breast cancer risk and appears to be unrelated to ovarian cancer risk

Outdoor Particulate Matter Exposure and Lung Cancer: A Systematic Review and Meta-Analysis

Background: Particulate matter (PM) in outdoor air pollution was recently designated a Group I carcinogen by the International Agency for Research on Cancer (IARC). This determination was based on the evidence regarding the relationship of PM2.5 and PM10 to lung cancer risk; however, the IARC evaluation did not include a quantitative summary of the evidence. Objective: Our goal was to provide a systematic review and quantitative summary of the evidence regarding the relationship between PM and lung cancer. Methods: We conducted meta-analyses of studies examining the relationship of exposure to PM2.5 and PM10 with lung cancer incidence and mortality. In total, 18 studies met our inclusion criteria and provided the information necessary to estimate the change in lung cancer risk per 10-μg/m3 increase in exposure to PM. We used random-effects analyses to allow between-study variability to contribute to meta-estimates. Results: The meta-relative risk for lung cancer associated with PM2.5 was 1.09 (95% CI: 1.04, 1.14). The meta-relative risk of lung cancer associated with PM10 was similar, but less precise: 1.08 (95% CI: 1.00, 1.17). Estimates were robust to restriction to studies that considered potential confounders, as well as subanalyses by exposure assessment method. Analyses by smoking status showed that lung cancer risk associated with PM2.5 was greatest for former smokers [1.44 (95% CI: 1.04, 1.22)], followed by never-smokers [1.18 (95% CI: 1.00, 1.39)], and then current smokers [1.06 (95% CI: 0.97, 1.15)]. In addition, meta-estimates for adenocarcinoma associated with PM2.5 and PM10 were 1.40 (95% CI: 1.07, 1.83) and 1.29 (95% CI: 1.02, 1.63), respectively. Conclusion: The results of these analyses, and the decision of the IARC Working Group to classify PM and outdoor air pollution as carcinogenic (Group 1), further justify efforts to reduce exposures to air pollutants that can arise from many sources. Citation: Hamra GB, Guha N, Cohen A, Laden F, Raaschou-Nielsen O, Samet JM, Vineis P, Forastiere F, Saldiva P, Yorifuji T, Loomis D. 2014. Outdoor particulate matter exposure and lung cancer: a systematic review and meta-analysis. Environ Health Perspect 122:906–911; http://dx.doi.org/10.1289/ehp.140809

Characterization of Residential Pesticide Use and Chemical Formulations through Self-Report and Household Inventory: The Northern California Childhood Leukemia Study

Background: Home and garden pesticide use has been linked to cancer and other health outcomes in numerous epidemiological studies. Exposure has generally been self-reported, so the assessment is potentially limited by recall bias and lack of information on specific chemicals. Objectives: As part of an integrated assessment of residential pesticide exposure, we identified active ingredients and described patterns of storage and use. Methods: During a home interview of 500 residentially stable households enrolled in the Northern California Childhood Leukemia Study during 2001–2006, trained interviewers inventoried residential pesticide products and queried participants about their storage and use. U.S. Environmental Protection Agency registration numbers, recorded from pesticide product labels, and pesticide chemical codes were matched to public databases to obtain information on active ingredients and chemical class. Poisson regression was used to identify independent predictors of pesticide storage. Analyses were restricted to 259 participating control households. Results: Ninety-five percent (246 of 259) of the control households stored at least one pesticide product (median, 4). Indicators of higher sociodemographic status predicted more products in storage. We identified the most common characteristics: storage areas (garage, 40%; kitchen, 20%), pests treated (ants, 33%; weeds, 20%), pesticide types (insecticides, 46%; herbicides, 24%), chemical classes (pyrethroids, 77%; botanicals, 50%), active ingredients (pyrethrins, 43%) and synergists (piperonyl butoxide, 42%). Products could contain multiple active ingredients. Conclusions: Our data on specific active ingredients and patterns of storage and use will inform future etiologic analyses of residential pesticide exposures from self-reported data, particularly among households with young children

The effect of occupational exposure to welding fumes on trachea, bronchus and lung cancer: A systematic review and meta-analysis from the WHO/ILO Joint Estimates of the Work-related Burden of Disease and Injury

Background: The World Health Organization (WHO) and the International Labour Organization (ILO) are the producers of the WHO/ILO Joint Estimates of the Work-related Burden of Disease and Injury (WHO/ILO Joint Estimates). Welding fumes have been classified as carcinogenic to humans (Group 1) by the WHO International Agency for Research on Cancer (IARC) in IARC Monograph 118; this assessment found sufficient evidence from studies in humans that welding fumes are a cause of lung cancer. In this article, we present a systematic review and meta-analysis of parameters for estimating the number of deaths and disability-adjusted life years from trachea, bronchus, and lung cancer attributable to occupational exposure to welding fumes, to inform the development of WHO/ILO Joint Estimates on this burden of disease (if considered feasible). Objectives: We aimed to systematically review and meta-analyse estimates of the effect of any (or high) occupational exposure to welding fumes, compared with no (or low) occupational exposure to welding fumes, on trachea, bronchus, and lung cancer (three outcomes: prevalence, incidence, and mortality). Data sources: We developed and published a protocol, applying the Navigation Guide as an organizing systematic review framework where feasible. We searched electronic databases for potentially relevant records from published and unpublished studies, including Medline, EMBASE, Web of Science, CENTRAL and CISDOC. We also searched grey literature databases, Internet search engines, and organizational websites; hand-searched reference lists of previous systematic reviews; and consulted additional experts. Study eligibility and criteria: We included working-age (≥15 years) workers in the formal and informal economy in any Member State of WHO and/or ILO but excluded children (<15 years) and unpaid domestic workers. We included randomized controlled trials, cohort studies, case-control studies, and other non-randomized intervention studies with an estimate of the effect of any (or high) occupational exposure to welding fumes, compared with occupational exposure to no (or low) welding fumes, on trachea, bronchus, and lung cancer (prevalence, incidence, and mortality). Study appraisal and synthesis methods: At least two review authors independently screened titles and abstracts against the eligibility criteria at a first review stage and full texts of potentially eligible records at a second stage, followed by extraction of data from qualifying studies. If studies reported odds ratios, these were converted to risk ratios (RRs). We combined all RRs using random-effects meta-analysis. Two or more review authors assessed the risk of bias, quality of evidence, and strength of evidence, using the Navigation Guide tools and approaches adapted to this project. Subgroup (e.g., by WHO region and sex) and sensitivity analyses (e.g., studies judged to be of “high”/“probably high” risk of bias compared with “low”/“probably low” risk of bias) were conducted. Results: Forty-one records from 40 studies (29 case control studies and 11 cohort studies) met the inclusion criteria, comprising over 1,265,512 participants (≥22,761 females) in 21 countries in three WHO regions (Region of the Americas, European Region, and Western Pacific Region). The exposure and outcome were generally assessed by job title or self-report, and medical or administrative records, respectively. Across included studies, risk of bias was overall generally probably low/low, with risk judged high or probably high for several studies in the domains for misclassification bias and confounding.Our search identified no evidence on the outcome of having trachea, bronchus, and lung cancer (prevalence). Compared with no (or low) occupational exposure to welding fumes, any (or high) occupational exposure to welding fumes increased the risk of acquiring trachea, bronchus, and lung cancer (incidence) by an estimated 48 % (RR 1.48, 95 % confidence interval [CI] 1.29–1.70, 23 studies, 57,931 participants, I2 24 %; moderate quality of evidence). Compared with no (or low) occupational exposure to welding fumes, any (or high) occupational exposure to welding fumes increased the risk dying from trachea, bronchus, and lung cancer (mortality) by an estimated 27 % (RR 1.27, 95 % CI 1.04–1.56, 3 studies, 8,686 participants, I2 0 %; low quality of evidence). Our subgroup analyses found no evidence for difference by WHO region and sex. Sensitivity analyses supported the main analyses. Conclusions: Overall, for incidence and mortality of trachea, bronchus, and lung cancer, we judged the existing body of evidence for human data as “sufficient evidence of harmfulness” and “limited evidence of harmfulness”, respectively. Occupational exposure to welding fumes increased the risk of acquiring and dying from trachea, bronchus, and lung cancer. Producing estimates for the burden of trachea, bronchus, and lung cancer attributable to any (or high) occupational exposure to welding fumes appears evidence-based, and the pooled effect estimates presented in this systematic review could be used as input data for the WHO/ILO Joint Estimates. Protocol identifier: https://doi.org/10.1016/j.envint.2020.106089

Carcinogenicity of consumption of red and processed meat

In October, 2015, 22 scientists from ten countries met at the International Agency for Research on Cancer (IARC) in Lyon, France, to evaluate the carcinogenicity of the consumption of red meat and processed meat. These assessments will be published in volume 114 of the IARC Monographs

Haplotypes of DNA repair and cell cycle control genes, X-ray exposure, and risk of childhood acute lymphoblastic leukemia

[[abstract]]Background: Acute leukemias of childhood are a heterogeneous group of malignancies characterized by cytogenetic abnormalities, such as translocations and changes in ploidy. These abnormalities may be influenced by altered DNA repair and cell cycle control processes. Methods: We examined the association between childhood acute lymphoblastic leukemia (ALL) and 32 genes in DNA repair and cell cycle pathways using a haplotype-based approach, among 377 childhood ALL cases and 448 controls enrolled during 1995-2002. Results: We found that haplotypes in APEX1, BRCA2, ERCC2, and RAD51 were significantly associated with total ALL, while haplotypes in NBN and XRCC4, and CDKN2A were associated with structural and numerical change subtypes, respectively. In addition, we observed statistically significant interaction between exposure to 3 or more diagnostic X-rays and haplotypes of XRCC4 on risk of structural abnormality-positive childhood ALL. Conclusions: These results support a role of altered DNA repair and cell cycle processes in the risk of childhood ALL, and show that this genetic susceptibility can differ by cytogenetic subtype and may be modified by exposure to ionizing radiation. To our knowledge, our study is the first to broadly examine the DNA repair and cell cycle pathways using a haplotype approach in conjunction with X-ray exposures in childhood ALL risk. If confirmed, future studies are needed to identify specific functional SNPs in the regions of interest identified in this analysis