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Each year, unspecified agents caused an estimated 38.4 million episodes of illness, resulting in 71,878 hospitalizations and 1,686 deaths.

Each year, 31 major known pathogens acquired in the United States caused an estimated 9.4 million episodes of foodborne illness. Additional episodes of illness were caused by unspecified agents, including known agents with insufficient data to estimate agent-specific illness, known agents not yet recognized as causing foodborne illness, substances known to be in food but of unproven pathogenicity, and unknown agents. To estimate these additional illnesses, we used data from surveys, hospital records, and death certificates to estimate illnesses, hospitalizations, and deaths from acute gastroenteritis and subtracted illnesses caused by known gastroenteritis pathogens. If the proportions acquired by domestic foodborne transmission were similar to those for known gastroenteritis pathogens, then an estimated 38.4 million (90% credible interval [CrI] 19.8–61.2 million) episodes of domestically acquired foodborne illness were caused by unspecified agents, resulting in 71,878 hospitalizations (90% CrI 9,924–157,340) and 1,686 deaths (90% CrI 369–3,338).

Each year, 31 pathogens caused 9.4 million episodes of foodborne illness, resulting in 55,961 hospitalizations and 1,351 deaths.

Estimates of foodborne illness can be used to direct food safety policy and interventions. We used data from active and passive surveillance and other sources to estimate that each year 31 major pathogens acquired in the United States caused 9.4 million episodes of foodborne illness (90% credible interval [CrI] 6.6–12.7 million), 55,961 hospitalizations (90% CrI 39,534–75,741), and 1,351 deaths (90% CrI 712–2,268). Most (58%) illnesses were caused by norovirus, followed by nontyphoidal Salmonella spp. (11%), Clostridium perfringens (10%), and Campylobacter spp. (9%). Leading causes of hospitalization were nontyphoidal Salmonella spp. (35%), norovirus (26%), Campylobacter spp. (15%), and Toxoplasma gondii (8%). Leading causes of death were nontyphoidal Salmonella spp. (28%), T. gondii (24%), Listeria monocytogenes (19%), and norovirus (11%). These estimates cannot be compared with prior (1999) estimates to assess trends because different methods were used. Additional data and more refined methods can improve future estimates.

TOC summary: These infections may account for 896 disability-adjusted life years per 1 million inhabitants annually.

The public health effects of illness caused by foodborne pathogens in Greece during 1996–2006 was quantified by using publicly available surveillance data, hospital statistics, and literature. Results were expressed as the incidence of different disease outcomes and as disability-adjusted life years (DALY), a health indicator combining illness and death estimates into a single metric. It has been estimated that each year ≈370,000 illnesses/million inhabitants are likely caused because of eating contaminated food; 900 of these illnesses are severe and 3 fatal, corresponding to 896 DALY/million inhabitants. Ill-defined intestinal infections accounted for the greatest part of reported cases and 27% of the DALY. Brucellosis, echinococcosis, salmonellosis, and toxoplasmosis were found to be the most common known causes of foodborne illnesses, being responsible for 70% of the DALY. Overall, the DALY metric provided a quantitative perspective on the impact of foodborne illness that may be useful for prioritizing food safety management targets.

The number of U.S. deaths by unknown foodborne agents warrants additional efforts to identify causal agent.

This study reviews the available evidence on unknown pathogenic agents transmitted in food and examines the methods that have been used to estimate that such agents cause 3,400 deaths per year in the United States. The estimate of deaths was derived from hospital discharge and death certificate data on deaths attributed to gastroenteritis of unknown cause. Fatal illnesses due to unknown foodborne agents do not always involve gastroenteritis, and gastroenteritis may not be accurately diagnosed or reported on hospital charts or death certificates. The death estimate consequently omitted deaths from unknown foodborne agents that do not cause gastroenteritis and likely overstated the number of deaths from agents that cause gastroenteritis. Although the number of deaths from unknown foodborne agents is uncertain, the possible economic cost of these deaths is so large that increased efforts to identify the causal agents are warranted.

A total of 12 federal agencies, plus their state counterparts, contribute to the regulatory snarl that governs the safety of the American food supply. With so much federal oversight, one might expect U.S. foods to be virtually risk-free. But this is hardly the case; contaminated food is responsible for 75 million illnesses, 325,000 hospitalizations, and 5,000 deaths in the United States each year. Recent reports from the General Accounting Office and the National Research Council claim that creation of a single agency with centralized authority is the best solution to U.S. food safety problems. Some experts agree that regulatory gaps in food safety highlight the need for centralized leadership, and that more money is necessary to fund the number of inspectors needed to adequately inspect the food supply before it reaches consumers. The single-agency concept has garnered congressional, industry, and scientific support, but the idea isn't without its skeptics, who believe that consolidating food safety under a single agency eliminates checks and balances offered by the current system and, more importantly, runs the risk of politicizing the agency.

Foodborne illnesses caused by microbial and chemical contaminants in food are a substantial health burden worldwide. In 2007, human vibriosis (non-cholera Vibrio infections) became a notifiable disease in the United States. In addition, Vibrio species are among the 31 major known pathogens transmitted through food in the United States. Diverse surveillance systems for foodborne pathogens also track outbreaks, illnesses, hospitalization and deaths due to non-cholera vibrios. Considering the recognition of vibriosis as a notifiable disease in the United States and the availability of diverse surveillance systems, there is a need for the development of easily deployed visualization and analysis approaches that can combine diverse data sources in an interactive manner. Current efforts to address this need are still limited. Visual analytics is an iterative process conducted via visual interfaces that involves collecting information, data preprocessing, knowledge representation, interaction, and decision making. We have utilized public domain outbreak and surveillance data sources covering 1973 to 2010, as well as visual analytics software to demonstrate integrated and interactive visualizations of data on foodborne outbreaks and surveillance of Vibrio species. Through the data visualization, we were able to identify unique patterns and/or novel relationships within and across datasets regarding (i) causative agent; (ii) foodborne outbreaks and illness per state; (iii) location of infection; (iv) vehicle (food) of infection; (v) anatomical site of isolation of Vibrio species; (vi) patients and complications of vibriosis; (vii) incidence of laboratory-confirmed vibriosis and V. parahaemolyticus outbreaks. The additional use of emerging visual analytics approaches for interaction with data on vibriosis, including non-foodborne related disease, can guide disease control and prevention as well as ongoing outbreak investigations.

Analysis of foodborne outbreaks shows how advances in viral diagnostics are clarifying the causes of foodborne outbreaks and determining the high impact of norovirus infections.

Efforts to prevent foodborne illness target bacterial pathogens, yet noroviruses (NoV) are suspected to be the most common cause of gastroenteritis. New molecular assays allow for better estimation of the role of NoV in foodborne illness. We analyzed 8,271 foodborne outbreaks reported to the Centers for Disease Control and Prevention from 1991 to 2000 and additional data from 6 states. The proportion of NoV-confirmed outbreaks increased from 1% in 1991 to 12% in 2000. However, from 1998 to 2000, 76% of NoV outbreaks were reported by only 11 states. In 2000, an estimated 50% of foodborne outbreaks in 6 states were attributable to NoV. NoV outbreaks were larger than bacterial outbreaks (median persons affected: 25 versus 15), and 10% of affected persons sought medical care; 1% were hospitalized. More widespread use of molecular assays will permit better estimates of the role of NoV illness and help direct efforts to control foodborne illness.

An estimated 4.0–6.9 million episodes of foodborne gastroenteritis occur in Australia each year.

We estimated for Australia the number of cases, hospitalizations, and deaths due to foodborne gastroenteritis in a typical year, circa 2000. The total amount of infectious gastroenteritis was measured by using a national telephone survey. The foodborne proportion was estimated from Australian data on each of 16 pathogens. To account for uncertainty, we used simulation techniques to calculate 95% credibility intervals (CrI). The estimate of incidence of gastroenteritis in Australia is 17.2 million (95% confidence interval 14.5–19.9 million) cases per year. We estimate that 32% (95% CrI 24%–40%) are foodborne, which equals 0.3 (95% CrI 0.2–0.4) episodes per person, or 5.4 million (95% CrI 4.0–6.9 million) cases annually in Australia. Norovirus, enteropathogenic Escherichia coli, Campylobacter spp., and Salmonella spp. cause the most illnesses. In addition, foodborne gastroenteritis causes ≈15,000 (95% CrI 11,000–18,000) hospitalizations and 80 (95% CrI 40–120) deaths annually. This study highlights global public health concerns about foodborne diseases and the need for standardized methods, including assessment of uncertainty, for international comparison.

Few data exist about perceptions regarding the etiology of foodborne illness. Among public health staff throughout Tennessee, the three pathogens most commonly believed to cause foodborne illness in the United States actually account for only 12% of disease. Fewer than 3% of respondents correctly identified the leading cause of foodborne illness.

We estimated the possible effects of the next influenza pandemic in the United States and analyzed the economic impact of vaccine-based interventions. Using death rates, hospitalization data, and outpatient visits, we estimated 89,000 to 207,000 deaths; 314,000 to 734,000 hospitalizations; 18 to 42 million outpatient visits; and 20 to 47 million additional illnesses. Patients at high risk (15% of the population) would account for approximately 84% of all deaths. The estimated economic impact would be US$71.3 to $166.5 billion, excluding disruptions to commerce and society. At $21 per vaccinee, we project a net savings to society if persons in all age groups are vaccinated. At $62 per vaccinee and at gross attack rates of 25%, we project net losses if persons not at high risk for complications are vaccinated. Vaccinating 60% of the population would generate the highest economic returns but may not be possible within the time required for vaccine effectiveness, especially if two doses of vaccine are required.

Outbreak investigations can identify industrial gaps and regulatory measures to protect food.

Listeria monocytogenes, a bacterial foodborne pathogen, can cause meningitis, bacteremia, and complications during pregnancy. This report summarizes listeriosis outbreaks reported to the Foodborne Disease Outbreak Surveillance System of the Centers for Disease Control and Prevention during 1998–2008. The study period includes the advent of PulseNet (a national molecular subtyping network for outbreak detection) in 1998 and the Listeria Initiative (enhanced surveillance for outbreak investigation) in 2004. Twenty-four confirmed listeriosis outbreaks were reported during 1998–2008, resulting in 359 illnesses, 215 hospitalizations, and 38 deaths. Outbreaks earlier in the study period were generally larger and longer. Serotype 4b caused the largest number of outbreaks and outbreak-associated cases. Ready-to-eat meats caused more early outbreaks, and novel vehicles (i.e., sprouts, taco/nacho salad) were associated with outbreaks later in the study period. These changes may reflect the effect of PulseNet and the Listeria Initiative and regulatory initiatives designed to prevent contamination in ready-to-eat meat and poultry products.

To estimate the global illness and deaths caused by rotavirus disease, we reviewed studies published from 1986 to 2000 on deaths caused by diarrhea and on rotavirus infections in children. We assessed rotavirus-associated illness in three clinical settings (mild cases requiring home care alone, moderate cases requiring a clinic visit, and severe cases requiring hospitalization) and death rates in countries in different World Bank income groups. Each year, rotavirus causes approximately 111 million episodes of gastroenteritis requiring only home care, 25 million clinic visits, 2 million hospitalizations, and 352,000–592,000 deaths (median, 440,000 deaths) in children <5 years of age. By age 5, nearly every child will have an episode of rotavirus gastroenteritis, 1 in 5 will visit a clinic, 1 in 60 will be hospitalized, and approximately 1 in 293 will die. Children in the poorest countries account for 82% of rotavirus deaths. The tremendous incidence of rotavirus disease underscores the urgent need for interventions, such as vaccines, to prevent childhood deaths in developing nations.

Diarrheal illness remains 1 of the top 5 causes of death in low-income and middle-income countries, especially for children <5 years of age. Introduction of universal childhood vaccination against rotaviruses has greatly reduced the incidence and severity of illness in upper-income and lower-income settings. For adults, norovirus is the leading cause of sporadic cases and outbreaks of diarrheal illness and is responsible for nearly 21 million episodes annually in the United States, of which 5.5 million are foodborne. Public health efforts to control and prevent norovirus illness have focused on rapid outbreak detection and source identification and control of transmission in institutional settings.

The incidence of acute episodes of intestinal infectious diseases in the United States was estimated through analysis of community-based studies and national interview surveys. Their differing results were reconciled by adjusting the study population age distributions in the community-based studies, by excluding those cases that also showed respiratory symptoms, and by accounting for structural differences in the surveys. The reconciliation process provided an estimate of 99 million acute cases of either vomiting or diarrhea, or both, each year in this country, half of which involved more than a full day of restricted activity. The analysis was limited to cases of acute gastrointestinal diseases with vomiting or diarrhea but without respiratory symptoms. Physicians were consulted for 8.2 million illnesses; 250,000 of these required hospitalization. In 1985, hospitalizations incurred $560 million in medical costs and $200 million in lost productivity. Nonhospitalized cases (7.9 million) for which physicians were consulted incurred $690 million in medical costs and $2.06 billion in lost productivity. More than 90 million cases for which no physician was consulted cost an estimated $19.5 billion in lost productivity. The estimates excluded such costs as death, pain and suffering, lost leisure time, financial losses to food establishments, and legal expenses. According to these estimates, medical costs and lost productivity from acute intestinal infectious diseases amount to a minimum of about $23 billion a year in the United States.

Surveillance was enhanced and a retrospective interview study performed in 1998-99 to determine incidence, causes, and costs of foodborne illnesses in Uppsala, Sweden. Sixty-eight percent of the detected foodborne illness incidents were single cases, and 32% were outbreaks. Most (85%) of the incidents came to the attention of the municipal authorities through telephone calls from affected persons. Calicivirus, Campylobacter spp., and Staphyloccocus aureus were the most common etiological agents; meat, meat products, and mixed dishes were the most implicated food categories. The incidence of foodborne illness was estimated to be 38 cases per 1,000 inhabitants per year. The estimated average costs per illness were 2,164 Swedish Krona (SEK) ($246) to society and 500 SEK ($57) to the patient. The annual cost of foodborne illnesses in Sweden was estimated to be 1,082 million SEK ($123 million).

Background

Prion diseases are a family of rare, progressive, neurodegenerative disorders that affect humans and animals. The most common form of human prion disease, Creutzfeldt-Jakob disease (CJD), occurs worldwide. Variant CJD (vCJD), a recently emerged human prion disease, is a zoonotic foodborne disorder that occurs almost exclusively in countries with outbreaks of bovine spongiform encephalopathy.

This study describes the occurrence and epidemiology of CJD and vCJD in the United States.

Methodology/Principal Findings

Analysis of CJD and vCJD deaths using death certificates of US residents for 1979–2006, and those identified through other surveillance mechanisms during 1996–2008. Since CJD is invariably fatal and illness duration is usually less than one year, the CJD incidence is estimated as the death rate. During 1979 through 2006, an estimated 6,917 deaths with CJD as a cause of death were reported in the United States, an annual average of approximately 247 deaths (range 172–304 deaths). The average annual age-adjusted incidence for CJD was 0.97 per 1,000,000 persons. Most (61.8%) of the CJD deaths occurred among persons ≥65 years of age for an average annual incidence of 4.8 per 1,000,000 persons in this population. Most deaths were among whites (94.6%); the age-adjusted incidence for whites was 2.7 times higher than that for blacks (1.04 and 0.40, respectively). Three patients who died since 2004 were reported with vCJD; epidemiologic evidence indicated that their infection was acquired outside of the United States.

Conclusion/Significance

Surveillance continues to show an annual CJD incidence rate of about 1 case per 1,000,000 persons and marked differences in CJD rates by age and race in the United States. Ongoing surveillance remains important for monitoring the stability of the CJD incidence rates, and detecting occurrences of vCJD and possibly other novel prion diseases in the United States.

Cardiovascular disease (CVD) is the leading cause of death of women in the United States and most of the developed world. The latest available data from the World Health Organization indicate that 16.6 million people around the globe die of CVD each year. World deaths from coronary heart disease (CHD) in 2002 totalled 7.2 million. One in seven women in Europe will die of CHD; in the United Kingdom > 1.2 million women are living with CHD. Despite advances in diagnosing and treating CHD, the disease accounts for the majority of CVD deaths in women in the United States, with more than 240 000 dying annually. Although coronary heart disease is the predominant cause of mortality for adult women in the United States, screening for coronary risk factors and coronary risk reduction interventions remains underused in women. In February of 2004, the American Heart Association published the first evidence‐based guidelines for CVD prevention in women, consisting of a set of clinical recommendations tailored to a woman's individual level of risk.

Food-borne diseases are estimated at 76 million illnesses and 5000 deaths every year in the United States with the greatest burden on young children, the elderly and immunocompromised populations. The impact of efficient food distribution systems and a truly global food supply ensures that outbreaks, previously sporadic and contained locally, are far more widespread and emerging pathogens have far more frequent infection opportunities. Enterohemorrhagic E. coli is an emerging food- and water-borne pathogen family whose Shiga-like toxins induce painful hemorrhagic colitis with potentially lethal complications of hemolytic uremic syndrome (HUS). The clinical manifestations of Shiga toxin-induced HUS overlap with other related syndromes yet molecular mechanisms differ considerably. As discussed herein, understanding these differences and the novel properties of the toxins is imperative for clinical management decisions, design of appropriate animal models, and choices of adjunctive therapeutics. The emergence of new strains with rapidly aggressive virulence makes clinical and research initiatives in this field a high public health priority.

Trypanosoma cruzi is the protozoan parasite that causes Chagas’ disease, a frequently fatal illness affecting the heart and gastrointestinal systems. An estimated 16 million to 18 million people in Latin America and 50,000 to 100,000 people in the United States are infected with this pathogen. Treatment options for T. cruzi infections are suboptimal due to the toxicities and limited effectiveness of the available drugs. Azole antimicrobial agents have been discovered to have antitrypanosomal activity by inhibition of ergosterol synthesis. The triazole itraconazole was recently shown to produce a parasitologic cure rate of 53% in chronically infected patients (W. Apt et al., Am. J. Trop. Med. Hyg. 59:133–138, 1998), a result which may lead to more use of this family of drugs for the treatment of T. cruzi infections. In the experiments reported on here, resistance to azoles was induced in vitro by serial passage of mammalian-stage parasites in the presence of fluconazole for 4 months. These parasites were cross resistant to the other azoles, ketoconazole, miconazole, and itraconazole. They remained susceptible to benznidazole and amphotericin B. The azole-resistant phenotype was stable for more than 2 months of in vitro serial passage without fluconazole. In addition, the parasites resisted treatment in mice receiving ketoconazole. The rapid development of azole resistance in T. cruzi in vitro suggests that resistance to azole drugs has the potential to occur in patients and may pose an impediment to the progress being made in the treatment of T. cruzi infection.

The epidemiology of foodborne disease is changing. New pathogens have emerged, and some have spread worldwide. Many, including Salmonella, Escherichia coli O157:H7, Campylobacter, and Yersinia enterocolitica, have reservoirs in healthy food animals, from which they spread to an increasing variety of foods. These pathogens cause millions of cases of sporadic illness and chronic complications, as well as large and challenging outbreaks over many states and nations. Improved surveillance that combines rapid subtyping methods, cluster identification, and collaborative epidemiologic investigation can identify and halt large, dispersed outbreaks. Outbreak investigations and case-control studies of sporadic cases can identify sources of infection and guide the development of specific prevention strategies. Better understanding of how pathogens persist in animal reservoirs is also critical to successful long-term prevention. In the past, the central challenge of foodborne disease lay in preventing the contamination of human food with sewage or animal manure. In the future, prevention of foodborne disease will increasingly depend on controlling contamination of feed and water consumed by the animals themselves.

Abstract

Mathematical models that estimate the proportion of foodborne illnesses attributable to food commodities at specific points in the food chain may be useful to risk managers and policy makers to formulate public health goals, prioritize interventions, and document the effectiveness of mitigations aimed at reducing illness. Using human surveillance data on laboratory-confirmed Salmonella infections from the Centers for Disease Control and Prevention and Salmonella testing data from U.S. Department of Agriculture Food Safety and Inspection Service's regulatory programs, we developed a point-of-processing foodborne illness attribution model by adapting the Hald Salmonella Bayesian source attribution model. Key model outputs include estimates of the relative proportions of domestically acquired sporadic human Salmonella infections resulting from contamination of raw meat, poultry, and egg products processed in the United States from 1998 through 2003. The current model estimates the relative contribution of chicken (48%), ground beef (28%), turkey (17%), egg products (6%), intact beef (1%), and pork (<1%) across 109 Salmonella serotypes found in food commodities at point of processing. While interpretation of the attribution estimates is constrained by data inputs, the adapted model shows promise and may serve as a basis for a common approach to attribution of human salmonellosis and food safety decision-making in more than one country.

Background

The US CDC estimates over 2 million foodborne illnesses are annually caused by 4 major enteropathogens: non-typhoid Salmonella spp., Campylobacter spp., Shigella spp. and Yersinia enterocoltica. While data suggest a number of costly and morbid chronic sequelae associated with these infections, pathogen-specific risk estimates are lacking. We utilized a US Department of Defense medical encounter database to evaluate the risk of several gastrointestinal disorders following select foodborne infections.

Methods

We identified subjects with acute gastroenteritis between 1998 to 2009 attributed to Salmonella (nontyphoidal) spp., Shigella spp., Campylobacter spp. or Yersinia enterocolitica and matched each with up to 4 unexposed subjects. Medical history was analyzed for the duration of military service time (or a minimum of 1 year) to assess for incident chronic gastrointestinal disorders. Relative risks were calculated using modified Poisson regression while controlling for the effect of covariates.

Results

A total of 1,753 pathogen-specific gastroenteritis cases (Campylobacter: 738, Salmonella: 624, Shigella: 376, Yersinia: 17) were identified and followed for a median of 3.8 years. The incidence (per 100,000 person-years) of PI sequelae among exposed was as follows: irritable bowel syndrome (IBS), 3.0; dyspepsia, 1.8; constipation, 3.9; gastroesophageal reflux disease (GERD), 9.7. In multivariate analyses, we found pathogen-specific increased risk of IBS, dyspepsia, constipation and GERD.

Conclusions

These data confirm previous studies demonstrating risk of chronic gastrointestinal sequelae following bacterial enteric infections and highlight additional preventable burden of disease which may inform better food security policies and practices, and prompt further research into pathogenic mechanisms.

Active Bacterial Core surveillance (ABCs) is a collaboration between the Centers for Disease Control and Prevention and several state health departments and universities participating in the Emerging Infections Program Network. ABCs conducts population-based active surveillance, collects isolates, and performs studies of invasive disease caused by Streptococcus pneumoniae, group A and group B Streptococcus, Neisseria meningitidis, and Haemophilus influenzae for a population of 17 to 30 million. These pathogens caused an estimated 97,000 invasive cases, resulting in 10,000 deaths in the United States in 1998. Incidence rates of these pathogens are described. During 1998, 25% of invasive pneumococcal infections in ABCs areas were not susceptible to penicillin, and 13.3% were not susceptible to three classes of antibiotics. In 1998, early-onset group B streptococcal disease had declined by 65% over the previous 6 years. More information on ABCs is available at www.cdc.gov/ncidod/dbmd/abcs. ABCs specimens will soon be available to researchers through an archive.

A hidden Markov model (HMM) has been developed to find protein coding genes in E. coli DNA using E. coli genome DNA sequence from the EcoSeq6 database maintained by Kenn Rudd. This HMM includes states that model the codons and their frequencies in E. coli genes, as well as the patterns found in the intergenic region, including repetitive extragenic palindromic sequences and the Shine-Delgarno motif. To account for potential sequencing errors and or frameshifts in raw genomic DNA sequence, it allows for the (very unlikely) possibility of insertions and deletions of individual nucleotides within a codon. The parameters of the HMM are estimated using approximately one million nucleotides of annotated DNA in EcoSeq6 and the model tested on a disjoint set of contigs containing about 325,000 nucleotides. The HMM finds the exact locations of about 80% of the known E. coli genes, and approximate locations for about 10%. It also finds several potentially new genes, and locates several places were insertion or deletion errors/and or frameshifts may be present in the contigs.

Background

There are an estimated 9.4 million cases of foodborne illness each year. Consumers have a key role in preventing foodborne illness, but differences in the practice of food safety behaviors exist, increasing risk for certain groups in the population. Identifying groups who are more likely to practice risky food safety behaviors can assist in development of interventions to reduce the disease burden of foodborne illnesses. The purpose of this investigation was to examine the relationships of health indicators and psychosocial factors with self-reported food safety behaviors.

Methods and Findings

Data were collected via questionnaire from 153 African Americans who attend churches in Baltimore City. Individuals reported high overall concern with food safety (mean score: 0.80±0.49 on a scale of −1 to +1) and practiced food safety behaviors with moderate overall frequency (mean score: 5.26±4.01 on a scale of −12 to +12), with considerable variation in reported frequencies depending on the food safety behavior. After adjusting for demographic variables, food safety behaviors were significantly associated with BMI and psychosocial variables. Riskier food safety behaviors were associated with higher body mass index (BMI) (β = −0.141 95%CI (−0.237, −0.044), p = 0.004). Self-efficacy for healthy eating (standard β [std. β] = 0.250, p = 0.005) and healthy eating intentions (std. β = 0.178, p = 0.041) were associated with better food safety behaviors scores.

Conclusions

These results show important relationships between weight-related health indicators, psychosocial factors and food safety behaviors that have not previously been studied. Interventions tailored to higher-risk populations have the potential to reduce the burden of food-related illnesses. Additional studies are needed to further investigate these relationships with larger and more diverse samples.