An appeal process for an injured worker compensation case is a unique opportunity to debate and integrate evidence concerning a potential causal relationship between observations of occupational disease and exposures to various putative risk factors that may also be of significance in public health protection. Through application of Hill’s indicia to the evidence presented in a recent appeal process concerning a breast cancer case for a female border guard, a novel epidemic, tentatively called “occupational BRCAness” has been identified and a causal relationship with exposures to traffic-related air pollution and shift work and possibly secondhand tobacco smoke is inferred. Application of the audit method by worker advocates to other compensation appeals processes for other diseases might similarly yield causal relations with exposures to occupational risk factors with relevance to public health.
BeckU.Risk society: towards a new modernity.
London:
SAGE, 1992.
2.
RutsteinDDMullanRJFrazierTMet al.
Sentinel health events (occupational): a basis for physician recognition and public health surveillance. Am J Public Health1983;
73: 1054–1062.
HillAB.The environment and disease: association or causation?Proc R Soc Med1965;
58: 295–300.
12.
U.S. Department of Health, Education, and Welfare. Smoking and health: report of the advisory committee to the surgeon general of the public health service.
Washington, DC:
U.S. Department of Health, Education, and Welfare, Public Health Service, Center for Disease Control, PHS Publication No. 1103, 1964.
13.
SusserM.The logic of Sir Karl Popper and the practice of epidemiology. Am J Epidemiol1986;
124: 711–718.
14.
PekkanenJPearceN.Environmental epidemiology: challenges and opportunities.Environ Health Perspect2001;
109: 1–5.
15.
KriegerN.Epidemiology and the web of causation: has anyone seen the spider?Soc Sci Med1994;
39: 887–903.
LuginaahINGoreyKMTangKet al.
Geographical analysis of breast cancer clustering in southern Ontario: generating hypotheses on environmental influences. Int J Environ Health Res2012;
22: 232–248.
LeeAJCunninghamAPKuchenbaeckerKBet al.
BOADICEA breast cancer risk prediction model: updates to cancer incidences, tumour pathology and web interface. Br J Cancer2014;
110: 535–545.
RussoJRussoIH.Experimentally induced mammary tumors in rats. Breast Cancer Res Treat1996;
39: 7–20.
26.
SenguptaP.The laboratory rat: relating its age with human’s. Int J Prev Med2013;
4: 624–630.
27.
ShahPNMhatreMCKothariLS.Effect of melatonin on mammary carcinogenesis in intact and pinealectomized rats in varying photoperiods. Cancer Res1984;
44: 3403–3407.
28.
KeramatiniaAHassanipourSNazarzadehMet al.
Correlation between nitrogen dioxide as an air pollution indicator and breast cancer: a systematic review and meta-analysis. Asian Pac J Cancer Prev2016;
17: 419–424.
29.
CrouseDLGoldbergMSRossNAet al.
Postmenopausal breast cancer is associated with exposure to traffic-related air pollution in Montreal, Canada: a case-control study. Environ Health Perspect2010;
118: 1578–1583.
30.
CrouseDLPetersPAVilleneuvePJet al.
Within- and between-city contrasts in nitrogen dioxide and mortality in 10 Canadian cities; a subset of the Canadian Census Health and Environment Cohort (CanCHEC). J Expo Sci Environ Epidemiol2015;
25: 482–489.
RhodesAJasaniBBalatonAJet al.
Immunohistochemical demonstration of oestrogen and progesterone receptors: correlation of standards achieved on in house tumours with that achieved on external quality assessment material in over 150 laboratories from 26 countries. J Clinical Pathol2000;
53: 292–301.
33.
SantagataSInceTA.Normal cell phenotypes of breast epithelial cells provide the foundation of a breast cancer taxonomy. Expert Rev Anticancer Ther2014;
14: 1385–1389.
LehmannBDBauerJAChenXet al.
Identification of human triple-negative breast cancer subtypes and preclinical models for selection of targeted therapies. J Clin Invest2011;
121: 2750–2767.
36.
LiuYRJiangYZXuXEet al.
Comprehensive transcriptome analysis identifies novel molecular subtypes and subtype-specific RNAs of triple-negative breast cancer. Breast Cancer Res2016;
18: 33.
37.
WormkeMStonerMSavilleBet al.
The aryl hydrocarbon receptor mediates degradation of estrogen receptor alpha through activation of proteasomes. Mol Cell Biol2003;
23: 1843–1855.
38.
GorskiJJKennedyRDHoseyAMet al.
The complex relationship between BRCA1 and ER alpha in hereditary breast cancer. Clin Cancer Res2009;
15: 1514–1518.
39.
TurnerNTuttAAshworthA.Hallmarks of ‘BRCAness’ in sporadic cancers. Nat Rev Cancer2004;
4: 814–819.
40.
HockingsJKThornePAKempMQet al.
The ligand status of the aromatic hydrocarbon receptor modulates transcriptional activation of BRCA-1 promoter by estrogen. Cancer Res2006;
66: 2224–2232.
41.
TanSLWChadhaSLiuYet al.
A class of environmental and endogenous toxins induces BRCA2 haploinsufficiency and genome instability. Cell2017;
169: 1105–1118.
42.
HanahanDWeinbergRA.Hallmarks of cancer: the next generation. Cell2011;
144: 646–674.
43.
GoodsonWHIIILoweLCarpenterDOet al.
Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead. Carcinogenesis2015;
36: S254–S296.
44.
RudelRAAttfieldKRSchifanoJNet al.
Chemicals causing mammary gland tumors in animals signal new directions for epidemiology, chemicals testing, and risk assessment for breast cancer prevention. Cancer2007;
109: 2635–2666.
45.
GrayJMRasanayagamSEngelCet al.
State of the evidence 2017: an update on the connection between breast cancer and the environment. Environ Health2017;
16: 94–155.
46.
BretonCVMarutaniAN.Air pollution and epigenetics: recent findings. Curr Environ Health Rep2014;
1: 35–45.
47.
NarodSA.Countercurrents: breast cancer and the environment: what is left to learn?Curr Oncol2012;
20: 8–9.
48.
KuhnTS.The structure of scientific revolutions. 1st ed.
Chicago, IL: University of Chicago Press. 1962.
