Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Mary Jo Reilly is active.

Publication


Featured researches published by Mary Jo Reilly.


Journal of Occupational and Environmental Medicine | 2006

How Much Work-related Injury and Illness is Missed By the Current National Surveillance System?

Kenneth D. Rosenman; Alice Kalush; Mary Jo Reilly; Joseph C. Gardiner; Mathew J. Reeves; Zhewui Luo

Objective: We sought to estimate the undercount in the existing national surveillance system of occupational injuries and illnesses. Methods: Adhering to the strict confidentiality rules of the U.S. Bureau of Labor Statistics, we matched the companies and individuals who reported work-related injuries and illnesses to the Bureau in 1999, 2000, and 2001 in Michigan with companies and individuals reported in four other Michigan data bases, workers’ compensation, OSHA Annual Survey, OSHA Integrated Management Information System, and the Occupational Disease Report. We performed capture–recapture analysis to estimate the number of cases missed by the combined systems. Results: We calculated that the current national surveillance system did not include 61% and with capture–recapture analysis up to 68% of the work-related injuries and illnesses that occurred annually in Michigan. This was true for injuries alone, 60% and 67%, and illnesses alone 66% and 69%, respectively. Conclusions: The current national system for work-related injuries and illnesses markedly underestimates the magnitude of these conditions. A more comprehensive system, such as the one developed for traumatic workplace fatalities, that is not solely dependent on employer based data sources is needed to better guide decision-making and evaluation of public health programs to reduce work-related conditions.


Journal of Occupational and Environmental Medicine | 2003

Cleaning products and work-related asthma.

Kenneth D. Rosenman; Mary Jo Reilly; Donald P. Schill; David Valiante; Jennifer Flattery; Robert Harrison; Florence Reinisch; Elise Pechter; Letitia Davis; Catharine Tumpowsky; Margaret S. Filios

To describe the characteristics of individuals with work-related asthma associated with exposure to cleaning products, data from the California-, Massachusetts-, Michigan-, and New Jersey state-based surveillance systems of work-related asthma were used to identify cases of asthma associated with exposure to cleaning products at work. From 1993 to 1997, 236 (12%) of the 1915 confirmed cases of work-related asthma identified by the four states were associated with exposure to cleaning products. Eighty percent of the reports were of new-onset asthma and 20% were work-aggravated asthma. Among the new-onset cases, 22% were consistent with reactive airways dysfunction syndrome. Individuals identified were generally women (75%), white non-Hispanic (68%), and 45 years or older (64%). Their most likely exposure had been in medical settings (39%), schools (13%), or hotels (6%), and they were most likely to work as janitor/cleaners (22%), nurse/nurses’ aides (20%), or clerical staff (13%). However, cases were reported with exposure to cleaning products across a wide range of job titles. Cleaning products contain a diverse group of chemicals that are used in a wide range of industries and occupations as well as in the home. Their potential to cause or aggravate asthma has recently been recognized. Further work to characterize the specific agents and the circumstances of their use associated with asthma is needed. Additional research to investigate the frequency of adverse respiratory effects among regular users, such as housekeeping staff, is also needed. In the interim, we recommend attention to adequate ventilation, improved warning labels and Material Safety Data Sheets, and workplace training and education.


Occupational and Environmental Medicine | 2004

A descriptive study of work aggravated asthma

S K Goe; Paul K. Henneberger; Mary Jo Reilly; Kenneth D. Rosenman; Donald P. Schill; David Valiante; Jennifer Flattery; Robert Harrison; Florence Reinisch; Catharine Tumpowsky; Margaret S. Filios

Background and Aims: Work related asthma (WRA) is one of the most frequently reported occupational lung diseases in a number of industrialised countries. A better understanding of work aggravated asthma (WAA), as well as work related new onset asthma (NOA), is needed to aid in prevention efforts. Methods: WAA and NOA in the United States were compared using cases reported to the National Institute for Occupational Safety and Health (NIOSH) from four state Sentinel Event Notification Systems for Occupational Risks (SENSOR) surveillance programmes for 1993–95. Results: A total of 210 WAA cases and 891 NOA cases were reported. WAA cases reported mineral and inorganic dusts as the most common exposure agent, as opposed to NOA cases, in which diisocyanates were reported most frequently. A similar percentage of WAA and NOA cases still experienced breathing problems at the time of the interview or had visited a hospital or emergency room for work related breathing problems. NOA cases were twice as likely to have applied for workers’ compensation compared with WAA cases. However, among those who had applied for worker compensation, approximately three-fourths of both WAA and NOA cases had received awards. The services and manufacturing industrial categories together accounted for the majority of both WAA (62%) and NOA (75%) cases. The risk of WAA, measured by average annual rate, was clearly the highest in the public administration (14.2 cases/105) industrial category, while the risk of NOA was increased in both the manufacturing (3.2 cases/105) and public administration (2.9 cases/105) categories. Conclusions: WAA cases reported many of the same adverse consequences as NOA cases. Certain industries were identified as potential targets for prevention efforts based on either the number of cases or the risk of WAA and NOA.


American Journal of Industrial Medicine | 1997

Work-related asthma and respiratory symptoms among workers exposed to metal-working fluids

Kenneth D. Rosenman; Mary Jo Reilly; Douglas J. Kalinowski

The objective of this work was to determine whether the prevalence of respiratory symptoms differed among workers exposed to different types of metal-working fluids. As part of a mandatory surveillance system for occupational illness, from 1988-1994, the Michigan Department of Public Health received, 86 occupational disease reports of work-related asthma secondary to exposure to metal-working fluids. As part of a public health program, follow-up industrial hygiene inspections, including medical interviews of the workforce, were performed at companies where the reported cases had become ill. Metal-working fluids were the second most common cause of work-related asthma reported in the state. Most of the reports were from the automobile industry. Follow-up inspections were conducted at 37 facilities where the individuals with work-related asthma had worked. Seven hundred and fifty-five workers at these facilities were interviewed. Only one facility was above the allowable oil mist standard. Despite the exposure levels being within the legal limits, approximately 20% of the fellow workers of the reported cases had daily or weekly respiratory symptoms suggestive of work-related asthma. Workers exposed to emulsified, semisynthetic, or synthetic machining coolants were more likely to have chronic bronchitis; to have visited a doctor for shortness of breath; to have visited a doctor for a sinus problem; to be bothered at work by nasal stuffiness, runny nose, or sore throat; and to have an increased prevalence of respiratory symptoms consistent with work-related asthma, compared to workers exposed to mineral oil metal-working fluids. These findings were found in individuals who currently smoked, had never smoked or were ex-cigarette smokers. Further research to determine the chemical components or microbial contaminants responsible for these findings is needed.


Environmental Health Perspectives | 2005

Chronic beryllium disease and sensitization at a beryllium processing facility.

Kenneth D. Rosenman; Vicki S. Hertzberg; Carol Rice; Mary Jo Reilly; Judith Aronchick; John E. Parker; Jackie Regovich; Milton D. Rossman

We conducted a medical screening for beryllium disease of 577 former workers from a beryllium processing facility. The screening included a medical and work history questionnaire, a chest radiograph, and blood lymphocyte proliferation testing for beryllium. A task exposure and a job exposure matrix were constructed to examine the association between exposure to beryllium and the development of beryllium disease. More than 90% of the cohort completed the questionnaire, and 74% completed the blood and radiograph component of the screening. Forty-four (7.6%) individuals had definite or probable chronic beryllium disease (CBD), and another 40 (7.0%) were sensitized to beryllium. The prevalence of CBD and sensitization in our cohort was greater than the prevalence reported in studies of other beryllium-exposed cohorts. Various exposure measures evaluated included duration; first decade worked; last decade worked; cumulative, mean, and highest job; and highest task exposure to beryllium (to both soluble and nonsoluble forms). Soluble cumulative and mean exposure levels were lower in individuals with CBD. Sensitized individuals had shorter duration of exposure, began work later, last worked longer ago, and had lower cumulative and peak exposures and lower nonsoluble cumulative and mean exposures. A possible explanation for the exposure–response findings of our study may be an interaction between genetic predisposition and a decreased permanence of soluble beryllium in the body. Both CBD and sensitization occurred in former workers whose mean daily working lifetime average exposures were lower than the current allowable Occupational Safety and Health Administration workplace air level of 2 μg/m3 and the Department of Energy guideline of 0.2 μg/m3.


Journal of Occupational and Environmental Medicine | 1998

Occupational noise-induced hearing loss surveillance in Michigan

Mary Jo Reilly; Kenneth D. Rosenman; Douglas J. Kalinowski

Occupational noise-induced hearing loss (NIHL) is an important yet often overlooked illness that can affect an individuals safety and performance at work. This article describes a state-based surveillance system for occupational NIHL. The Michigan surveillance system enables us to describe the magnitude of occupational NIHL among Michigan workers and direct public health interventions in the form of enforcement workplace inspections. The data presented are based on interviews of individuals with occupational NIHL reported to the Michigan Department of Consumer and Industry Services (MDCIS) by Michigans audiologists and otolaryngologists from 1992-1997. From 1992-1997, 1378 individuals with occupational NIHL were reported to the MDCIS and interviewed about their exposures to noise at work. Over 70% of the workplace noise exposure were in manufacturing. At the most recent company where these individuals were exposed to noise, approximately 46% were not provided regular hearing testing. Regular hearing testing was more likely to occur in the larger companies and in industries covered by regulations requiring such testing to be performed. There were improvements over time in the percentages of companies providing regular hearing testing and hearing protection. Construction workers are employees among a group of industries that are not adequately protected from excessive noise exposures by occupational regulations. Regular hearing testing was not provided for over 90% of construction jobs, although hearing protection such as earplugs or earmuffs was provided for approximately half of these jobs. Forty-three state enforcement inspections were conducted at the companies reported by the patients interviewed, because these companies were reported to provide no regular hearing testing or no hearing protection despite exposures to excessive levels of noise. During the 43 inspections, 23 companies had noise levels above dBA, and 17 of those had either no hearing conservation program (HCP) or had one that was cited as being incomplete. The inspections potentially protected 758 similarly exposed workers in the companies with the high noise levels that lacked an HCP or that had a deficient HCP. The number of patients with occupational NIHL is likely a gross underestimate of the true magnitude of the disease. However, the surveillance system has identified workplaces with hazardous levels of noise and no HCP, thereby protecting similarly exposed coworkers of the index patients from further exposures to noise and hearing loss.


Journal of Occupational and Environmental Medicine | 2003

Work-related reactive airways dysfunction syndrome cases from surveillance in selected US states.

Paul K. Henneberger; Susan J. Derk; Letitia Davis; Catharine Tumpowsky; Mary Jo Reilly; Kenneth D. Rosenman; Donald P. Schill; David Valiante; Jennifer Flattery; Robert Harrison; Florence Reinisch; Margaret S. Filios; Brian Tift

Learning ObjectivesDistinguish between reactive airways dysfunction syndrome (RADS) and other cases of work-related asthma (WRA) associated with a known asthma-inducing agent.Contrast the clinical features, severity, and course of RADS with those of other WRA related to an identified asthma inducer.Identify differences in outcome and disposition between RADS and other WRA. The objective was to elaborate the descriptive epidemiology of work-related cases of reactive airways dysfunction syndrome (RADS). Cases of work-related asthma (WRA) were identified in four states in the United States during 1993–1995 as part of the Sentinel Event Notification Systems for Occupational Risks (SENSOR). Information gathered by follow-back interview was used to describe 123 work-related RADS cases and to compare them to 301 other WRA cases whose onset of disease was associated with a known asthma inducer. RADS represented 14% of all new-onset WRA cases identified by the state SENSOR surveillance systems. RADS cases had significant adverse medical and occupational outcomes identified by follow-back interview. In particular, 89% still had breathing problems, 78% had ever sought emergency care and 39% had ever been hospitalized for work-related breathing problems, 54% had applied for worker compensation benefits, and 41% had left the company where they experienced onset of asthma. These values equaled or exceeded the comparable figures for those WRA cases whose onset was attributed to a known inducer. Work-related RADS represents a minority of all WRA cases, but the adverse impact of this condition appears to equal that of other WRA cases.


Occupational and Environmental Medicine | 2011

HLA class II DPB1 and DRB1 polymorphisms associated with genetic susceptibility to beryllium toxicity

Kenneth D. Rosenman; Milton D. Rossman; Vicki S. Hertzberg; Mary Jo Reilly; Carol Rice; E Kanterakis; Dimitri Monos

Objectives Chronic beryllium disease (CBD) is a hypersensitivity granulomatous pulmonary disease caused by exposure to the metal beryllium (Be2+). Our objective was to extend current knowledge of the genetics of beryllium disease by examining all HLA-DPB1 and HLA-DPR1 gene polymorphisms and the interactions between them. Methods DNA-based typing of HLA-DPB1 and HLA-DRB1 loci at the allele level was performed on 65 CBD, 44 beryllium sensitised (BeS) but without CBD and 288 non-affected, beryllium exposed controls. Results The DPβE69 residue regardless of zygosity, but particularly if present on non-*0201 alleles, was of primary importance for the development of CBD and BeS, while other negatively charged residues DPβDE55, 56 and DPβDE84, 85 incrementally increased, although not independently, the risk. The DPβE69 positive alleles with charge −7 or −9 were associated with both CBD and BeS. The polymorphic residues DPβE69, DPβDE55, 56 and DPβDE84, 85 were responsible for the −9 charge and the first two residues for the −7 charge. Conclusions In the absence of DPβE69, DRβE71 is a risk factor for CBD and BeS. DPβE69 and DRβE71 are adjacent to other amino acids that are also negatively charged, suggesting that the positively charged Be2+ modifies the local environment of the epitopes in a way that promotes interactions between peptides and T cells and results in CBD. Finally, the protective effect of the DPB1*0201 positive haplotype may involve particular polymorphisms outside of the DPB1 gene.


Nephron | 2000

Kidney Disease and Silicosis

Kenneth D. Rosenman; M. Moore-Fuller; Mary Jo Reilly

Aim: To determine the prevalence of kidney disease in a cohort of individuals with silicosis. Methods: Review of medical records and questionnaires from patients reported to a state surveillance system for silicosis. Reporting of individuals with silicosis is required by state law. All individuals with silicosis reported as required by law to the State of Michigan. Individuals included in this article were reported from 1987 to 1995. Cases were reported by hospitals, physicians, the state workers’ compensation bureau, or from death certificates. Only individuals who met the criteria for silicosis developed by the National Institute for Occupational Safety and Health (NIOSH) were included. Results: Medical records were reviewed of 583 individuals with confirmed silicosis. This was mainly a population of elderly men. Ten percent of the 583 silicotics were found to have some mention of chronic kidney disease, and 33% of the 283 silicotics who we had laboratory tests on had a serum creatinine level >1.5 mg/dl. An association between kidney disease and age and between kidney disease and race was found among this cohort of 583 silicotics. Individuals with silicosis were more likely to have a serum creatinine level >1.5 mg/dl than age- and race-matched controls. However, no relationship between duration of exposure to silica or profusion of scarring on chest X-ray and prevalence of kidney disease or elevated creatinine levels was found. Conclusions: This study confirms previous case reports and epidemiologic studies of end-stage renal disease that found an association between kidney disease and exposure to silica. The epidemiologic data are conflicting on the mechanism by which silica causes kidney disease and are compatible with silica being able to cause kidney disease by both an autoimmune and direct nephrotoxic effect. Chronic kidney disease should be considered as a complication of silicosis.


Morbidity and Mortality Weekly Report | 2016

Surveillance for Silicosis — Michigan and New Jersey, 2003–2011

Patricia L. Schleiff; Jacek M. Mazurek; Mary Jo Reilly; Kenneth D. Rosenman; Martha B. Yoder; Margaret Lumia; Karen Worthington

CDCs National Institute for Occupational Safety and Health (NIOSH), state health departments, and other state entities maintain a state-based surveillance program of confirmed silicosis cases. Data on confirmed cases are collected and compiled by state entities and submitted to CDC. This report summarizes information for cases of silicosis that were reported to CDC for 2003-2011 by Michigan and New Jersey, the only states that continue to provide data voluntarily to NIOSH. The data for this report were final as of January 8, 2015. Data are presented in tabular form on the number and distribution of cases of silicosis by year (Table 1), duration of employment in occupations with potential exposure to dust containing respirable crystalline silica (Table 2), industry (Table 3), and occupation (Table 4). The number of cases by year is presented graphically (Figure). This report is a part of the Summary of Notifiable Noninfectious Conditions and Disease Outbreaks - United States, which encompasses various surveillance years but is being published in 2016 (1). The Summary of Notifiable Noninfectious Conditions and Disease Outbreaks appears in the same volume of MMWR as the annual Summary of Notifiable Infectious Diseases (2).

Collaboration


Dive into the Mary Jo Reilly's collaboration.

Top Co-Authors

Avatar
Top Co-Authors

Avatar

Robert Harrison

California Department of Public Health

View shared research outputs
Top Co-Authors

Avatar

Margaret S. Filios

National Institute for Occupational Safety and Health

View shared research outputs
Top Co-Authors

Avatar

Donald P. Schill

New Jersey Department of Health and Senior Services

View shared research outputs
Top Co-Authors

Avatar

Letitia Davis

Massachusetts Department of Public Health

View shared research outputs
Top Co-Authors

Avatar

David Valiante

New Jersey Department of Health and Senior Services

View shared research outputs
Top Co-Authors

Avatar

Carol Rice

University of Cincinnati

View shared research outputs
Top Co-Authors

Avatar

Catharine Tumpowsky

Massachusetts Department of Public Health

View shared research outputs
Top Co-Authors

Avatar

Elise Pechter

Massachusetts Department of Public Health

View shared research outputs
Top Co-Authors

Avatar
Researchain Logo
Decentralizing Knowledge