Tom Sorahan

Prof. Tom Sorahan


Research Focus & Metrics

Academic Career Length

46Years (1981-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 October 2011 in Bulletin of the World Health Organization
Verified
Journal Article
Closed access
VDVanya Delgermaa
Vanya Delgermaa
KTKen Takahashi
Ken Takahashi
EPEun-Kee Park
Eun-Kee Park
GLGiang Vinh Le
Giang Vinh Le
THToshiyuki Hara
Toshiyuki Hara
TSTom Sorahan
Tom Sorahan
To carry out a descriptive analysis of mesothelioma deaths reported worldwide between 1994 and 2008. We extracted data on mesothelioma deaths reported to the World Health Organization mortality database since 1994, when the disease was first recorded. We also sought information from other English-language sources. Crude and age-adjusted mortality rates were calculated and mortality trends were assessed from the annual percentage change in the age-adjusted mortality rate. In total, 92,253 mesothelioma deaths were reported by 83 countries. Crude and age-adjusted mortality rates were 6.2 and 4.9 per million population, respectively. The age-adjusted mortality rate increased by 5.37% per year and consequently more than doubled during the study period. The mean age at death was 70 years and the male-to-female ratio was 3.6:1. The disease distribution by anatomical site was: pleura, 41.3%; peritoneum, 4.5%; pericardium, 0.3%; and unspecified sites, 43.1%. The geographical distribution of deaths was skewed towards high-income countries: the United States of America reported the highest number, while over 50% of all deaths occurred in Europe. In contrast, less than 12% occurred in middle- and low-income countries. The overall trend in the age-adjusted mortality rate was increasing in Europe and Japan but decreasing in the United States. The number of mesothelioma deaths reported and the number of countries reporting deaths increased during the study period, probably due to better disease recognition and an increase in incidence. The different time trends observed between countries may be an early indication that the disease burden is slowly shifting towards those that have used asbestos more recently.

1 April 2011 in Environmental Health Perspectives
Verified
Journal Article
Open access
EPEun-Kee Park
Eun-Kee Park
KTKen Takahashi
Ken Takahashi
THTsutomu Hoshuyama
Tsutomu Hoshuyama
TCTsun-Jen Cheng
Tsun-Jen Cheng
VDVanya Delgermaa
Vanya Delgermaa
TSTom Sorahan
Tom Sorahan
A peer-reviewed open access journal published by the National Institute of Environmental Health Sciences

2 September 2017 in Occupational and Environmental Medicine
Verified
Journal Article
Open access
PDF file
COChimed-Ochir Odgerel
Chimed-Ochir Odgerel
KTKen Takahashi
Ken Takahashi
TSTom Sorahan
Tom Sorahan
TDTim Driscoll
Tim Driscoll
CFChristina Fitzmaurice
Christina Fitzmaurice
JTJukka Takala
Jukka Takala
Background Mesothelioma is increasingly recognised as a global health issue and the assessment of its global burden is warranted. Objectives To descriptively analyse national mortality data and to use reported and estimated data to calculate the global burden of mesothelioma deaths. Methods For the study period of 1994 to 2014, we grouped 230 countries into 59 countries with quality mesothelioma mortality data suitable to be used for reference rates, 45 countries with poor quality data and 126 countries with no data, based on the availability of data in the WHO Mortality Database. To estimate global deaths, we extrapolated the gender-specific and age-specific mortality rates of the countries with quality data to all other countries. Results The global numbers and rates of mesothelioma deaths have increased over time. The 59 countries with quality data recorded 15 011 mesothelioma deaths per year over the 3 most recent years with available data (equivalent to 9.9 deaths per million per year). From these reference data, we extrapolated the global mesothelioma deaths to be 38 400 per year, based on extrapolations for asbestos use. Conclusions Although the validity of our extrapolation method depends on the adequate identification of quality mesothelioma data and appropriate adjustment for other variables, our estimates can be updated, refined and verified because they are based on commonly accessible data and are derived using a straightforward algorithm. Our estimates are within the range of previously reported values but higher than the most recently reported values.

31 May 2012 in European Respiratory Journal
Verified
Journal Article
Open access
PDF file
OKOm Prakash Kurmi
Om Prakash Kurmi
PAPallavi Huma Arya
Pallavi Huma Arya
KLKin-Bong Hubert Lam
Kin-Bong Hubert Lam
TSTom Sorahan
Tom Sorahan
JAJon G. Ayres
Jon G. Ayres
The aim of this systematic review was to quantify the impact of biomass fuel and coal use on lung cancer and to explore reasons for heterogeneity in the reported effect sizes.A systematic review of primary studies reporting the relationship between solid fuel use and lung cancer was carried out, based on pre-defined criteria. Studies that dealt with confounding factors were used in the meta-analysis. Fuel types, smoking, country, cancer cell type and sex were considered in sub-group analyses. Publication bias and heterogeneity were estimated.The pooled effect estimate for coal smoke as a lung carcinogen (OR 1.82, 95% CI 1.60–2.06) was greater than that from biomass smoke (OR 1.50, 95% CI 1.17–1.94). The risk of lung cancer from solid fuel use was greater in females (OR 1.81, 95% CI 1.54–2.12) compared to males (OR 1.16, 95% CI 0.79–1.69). The pooled effect estimates were 2.33 (95% CI 1.72–3.17) for adenocarcinoma, 3.58 (1.58–8.12) for squamous cell carcinoma and 1.57 (1.38–1.80) for tumours of unspecified cell type.These findings suggest that in-home burning of both coal and biomass is consistently associated with an increased risk of lung cancer.

28 September 2016 in Critical Reviews in Toxicology
Verified
Journal Article
Open access
GWGary M. Williams
Gary M. Williams
MAMarilyn Aardema
Marilyn Aardema
JAJohn Acquavella
John Acquavella
SBSir Colin Berry
Sir Colin Berry
DBDavid Brusick
David Brusick
DWDouglas L. Weed
Douglas L. Weed
The International Agency for Research on Cancer (IARC) published a monograph in 2015 concluding that glyphosate is "probably carcinogenic to humans" (Group 2A) based on limited evidence in humans and sufficient evidence in experimental animals. It was also concluded that there was strong evidence of genotoxicity and oxidative stress. Four Expert Panels have been convened for the purpose of conducting a detailed critique of the evidence in light of IARC's assessment and to review all relevant information pertaining to glyphosate exposure, animal carcinogenicity, genotoxicity, and epidemiologic studies. Two of the Panels (animal bioassay and genetic toxicology) also provided a critique of the IARC position with respect to conclusions made in these areas. The incidences of neoplasms in the animal bioassays were found not to be associated with glyphosate exposure on the basis that they lacked statistical strength, were inconsistent across studies, lacked dose-response relationships, were not associated with preneoplasia, and/or were not plausible from a mechanistic perspective. The overall weight of evidence from the genetic toxicology data supports a conclusion that glyphosate (including GBFs and AMPA) does not pose a genotoxic hazard and therefore, should not be considered support for the classification of glyphosate as a genotoxic carcinogen. The assessment of the epidemiological data found that the data do not support a causal relationship between glyphosate exposure and non-Hodgkin's lymphoma while the data were judged to be too sparse to assess a potential relationship between glyphosate exposure and multiple myeloma. As a result, following the review of the totality of the evidence, the Panels concluded that the data do not support IARC's conclusion that glyphosate is a "probable human carcinogen" and, consistent with previous regulatory assessments, further concluded that glyphosate is unlikely to pose a carcinogenic risk to humans.

22 January 2004 in Occupational and Environmental Medicine
Verified
Journal Article
Open access
PDF file
TSTom Sorahan
Tom Sorahan
NEN A Esmen
N A Esmen
Aims:To investigate mortality from lung cancer in nickel-cadmium battery workers in relation to cumulative exposure to cadmium hydroxide.Methods:The mortality of a cohort of 926 male workers from a factory engaged in the manufacture of nickel-cadmium batteries in the West Midlands of England was investigated for the period 1947–2000. All subjects were first employed at the plant in the period 1947–75 and employed for a minimum period of 12 months. Work histories were available for the period 1947–86; the factory closed down in 1992. Two analytical approaches were used, indirect standardisation and Poisson regression.Results:Based on serial mortality rates for the general population of England and Wales, significantly increased mortality was shown for cancers of the pharynx (observed (Obs) 4, expected (Exp) 0.7, standardised mortality ratio (SMR) 559, p<0.05), non-malignant diseases of the respiratory system (Obs 61, Exp 43.0, SMR 142, p<0.05), and non-malignant diseases of the genitourinary system (Obs 10, Exp 4.1, SMR 243, p<0.05). Non-significantly increased SMRs were shown for lung cancer (Obs 45, Exp 40.7, SMR 111) and cancer of the prostate (Obs 9, Exp 7.5, SMR 116). Estimated cumulative cadmium exposures were not related to risks of lung cancer or risks of chronic obstructive pulmonary diseases, even when exposure histories were lagged first by 10, then by 20 years.Conclusions:The study findings do not support the hypotheses that cadmium compounds are human lung carcinogens.