Hassan Vally

Clinical effects of sulphite additives

Sulphites are widely used as preservative and antioxidant additives in the food and pharmaceutical industries. Topical, oral or parenteral exposure to sulphites has been reported to induce a range of adverse clinical effects in sensitive individuals, ranging from dermatitis, urticaria, flushing, hypotension, abdominal pain and diarrhoea to life‐threatening anaphylactic and asthmatic reactions. Exposure to the sulphites arises mainly from the consumption of foods and drinks that contain these additives; however, exposure may also occur through the use of pharmaceutical products, as well as in occupational settings. While contact sensitivity to sulphite additives in topical medications is increasingly being recognized, skin reactions also occur after ingestion of or parenteral exposure to sulphites. Most studies report a 3–10% prevalence of sulphite sensitivity among asthmatic subjects following ingestion of these additives. However, the severity of these reactions varies, and steroid‐dependent asthmatics, those with marked airway hyperresponsiveness, and children with chronic asthma, appear to be at greater risk. In addition to episodic and acute symptoms, sulphites may also contribute to chronic skin and respiratory symptoms. To date, the mechanisms underlying sulphite sensitivity remain unclear, although a number of potential mechanisms have been proposed. Physicians should be aware of the range of clinical manifestations of sulphite sensitivity, as well as the potential sources of exposure. Minor modifications to diet or behaviour lead to excellent clinical outcomes for sulphite‐sensitive individuals.

The prevalence of aspirin intolerant asthma (AIA) in Australian asthmatic patients

Background: Aspirin intolerant asthma (AIA) is a clinically distinct syndrome characterised by the precipitation of asthma attacks following the ingestion of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs). The prevalence of AIA among Australian asthmatic patients has not previously been reported. Methods: Three populations were surveyed to establish the prevalence of AIA among Australian asthmatics. Two surveys were completed in patients recruited from the metropolitan area in Perth, Western Australia, one comprising 150 recruited from hospital based sources (hospital cohort) and the second comprising 366 from the membership of the Asthma Foundation of Western Australia (Asthma Foundation cohort). In a third study 1298 individuals were randomly selected from the rural community of Busselton in Western Australia. Results: The prevalence of AIA in the hospital and Asthma Foundation cohorts was found to be 10.7% and 10.4%, respectively. Univariate analyses in the Asthma Foundation cohort indicated that AIA was associated with more severe asthma (OR = 2.4, 95% CI 1.18 to 4.86), nasal polyposis (OR=3.19, 95% CI 1.52 to 6.68), atopy (OR=2.96, 95% CI 1.48 to 5.89), sulfite sensitivity (OR=3.97, 95% CI 1.87 to 8.41), and sensitivity to wine (OR=3.27, 95% CI 1.65 to 6.47). Multivariate analyses indicated that atopy (OR=2.80, 95% CI 1.38 to 5.70), nasal polyposis (OR=3.39, 95% CI 1.57 to 7.29), and the number of asthma attacks in the previous 12 months (OR=1.20, 95% CI 1.02 to 1.42) were independent predictors for AIA, as was wine sensitivity (OR=2.20, 95% CI 1.02 to 4.72). The prevalence of AIA among asthmatic patients in the Busselton cohort was 10.9%. In addition, 2.5% of non-diagnosed asthmatics in this cohort reported asthma symptoms following aspirin ingestion. Conclusion: The prevalence of respiratory symptoms triggered by aspirin/NSAID use was found to be 10–11% in patients with asthma and 2.5% in non-asthmatics. Aspirin sensitivity appears to be a significant problem in the community and further investigations of the mechanisms of these responses and the possible link between this syndrome and other food and chemical sensitivities are required.

Role of sulfite additives in wine induced asthma: single dose and cumulative dose studies

BACKGROUND Wine appears to be a significant trigger for asthma. Although sulfite additives have been implicated as a major cause of wine induced asthma, direct evidence is limited. Two studies were undertaken to assess sulfite reactivity in wine sensitive asthmatics. The first study assessed sensitivity to sulfites in wine using a single dose sulfited wine challenge protocol followed by a double blind, placebo controlled challenge. In the second study a cumulative dose sulfited wine challenge protocol was employed to establish if wine sensitive asthmatics as a group have an increased sensitivity to sulfites. METHODS In study 1, 24 asthmatic patients with a strong history of wine induced asthma were screened. Subjects showing positive responses to single blind high sulfite (300 ppm) wine challenge were rechallenged on separate days in a double blind, placebo controlled fashion with wines of varying sulfite levels to characterise their responses to these drinks. In study 2, wine sensitive asthmatic patients (n=12) and control asthmatics (n=6) were challenged cumulatively with wine containing increasing concentrations of sulfite in order to characterise further their sensitivity to sulfites in wine. RESULTS Four of the 24 self-reporting wine sensitive asthmatic patients were found to respond to sulfite additives in wine when challenged in a single dose fashion (study 1). In the double blind dose-response study all four had a significant fall in forced expiratory volume in one second (FEV1) (>15% from baseline) following exposure to wine containing 300 ppm sulfite, but did not respond to wines containing 20, 75 or 150 ppm sulfite. Responses were maximal at 5 minutes (mean (SD) maximal decline in FEV1 28.7 (13)%) and took 15–60 minutes to return to baseline levels. In the cumulative dose-response study (study 2) no significant difference was observed in any of the lung function parameters measured (FEV1, peak expiratory flow (PEF), mid phase forced expiratory flow (FEF25–75)) between wine sensitive and normal asthmatic subjects. CONCLUSIONS Only a small number of wine sensitive asthmatic patients responded to a single dose challenge with sulfited wine under laboratory conditions. This may suggest that the role of sulfites and/or wine in triggering asthmatic responses has been overestimated. Alternatively, cofactors or other components in wine may play an important role in wine induced asthma. Cumulative sulfite dose challenges did not detect an increased sensitivity to sulfite in wine sensitive asthmatics and an alternative approach to identifying sulfite/wine sensitive asthma may be required.

Pentavalent rotavirus vaccine and prevention of gastroenteritis hospitalizations in Australia.

OBJECTIVE: A publicly funded, universal infant pentavalent rotavirus vaccine (RV5) program was implemented in Queensland, Australia, in mid-2007. We sought to assess vaccine effectiveness (VE) of 3 doses of RV5 at preventing rotavirus and nonrotavirus acute gastroenteritis (AGE) hospitalizations in the first birth cohort and impact on hospitalizations in all age groups. METHODS: Hospitalization rates for rotavirus and nonrotavirus AGE in all age groups before and after RV5 introduction were compared. Population vaccine coverage, hospitalization data, and individual vaccination status were obtained from routinely collected, publicly funded state- and nationally based data sets. Data linkage was performed to calculate 3-dose VE for preventing hospitalization in the eligible age group. RESULTS: RV5 coverage in the first eligible birth cohort was 89.6% for at least 1 dose and 73.1% for 3 doses. Three-dose VE for preventing nonrotavirus AGE hospitalization was 62.3% to 63.9% (any/primary diagnosis) and 89.3% to 93.9% (any/primary diagnosis) for rotavirus hospitalizations. After program implementation, there were immediate and sustained reductions in rotavirus hospitalizations for those who were younger than 20 years and nonrotavirus AGE-coded hospitalizations for those who were younger than 5 years. CONCLUSIONS: RV5 is highly effective at preventing rotavirus hospitalizations in a developed country setting, confirming efficacy figures from the pivotal clinical trial. Additional direct and indirect effects are substantial and include reductions in nonrotavirus AGE hospitalizations in vaccinated age groups and rotavirus and nonrotavirus AGE hospitalization rates in older age groups.

A Multistate Outbreak of Hepatitis A Associated With Semidried Tomatoes in Australia, 2009

BACKGROUND A large outbreak of hepatitis A affected individuals in several Australian states in 2009, resulting in a 2-fold increase in cases reported to state health departments compared with 2008. Two peaks of infection occurred (April-May and September-November), with surveillance data suggesting locally acquired infections from a widely distributed food product. METHODS Two case-control studies were completed. Intensive product trace-back and food sampling was undertaken. Genotyping was conducted on virus isolates from patient serum and food samples. Control measures included prophylaxis for close contacts, public health warnings, an order by the chief health officer under the Victorian Food Act 1984, and trade-level recalls on implicated batches of semidried tomatoes. RESULTS A multijurisdictional case-control study in April-May found an association between illness and consumption of semidried tomatoes (odds ratio [OR], 3.0; 95% CI 1.4-6.7). A second case-control study conducted in Victoria in October-November also implicated semidried tomatoes as being associated with illness (OR, 10.3; 95% CI, 4.7-22.7). Hepatitis A RNA was detected in 22 samples of semidried tomatoes. Hepatitis A virus genotype IB was identified in 144 of 153 (94%) patients tested from 2009, and partial sequence analysis showed complete identity with an isolate found in a sample of semidried tomatoes. CONCLUSIONS The results of both case-control studies and food testing implicated the novel vehicle of semidried tomatoes as the cause of this hepatitis A outbreak. The outbreak was extensive and sustained despite public health interventions, the design and implementation of which were complicated by limitations in food testing capability and complex supply chains.

Epidemiology of Shiga toxin producing Escherichia coli in Australia, 2000-2010

BackgroundShiga toxin-producing Escherichia coli (STEC) are an important cause of gastroenteritis in Australia and worldwide and can also result in serious sequelae such as haemolytic uraemic syndrome (HUS). In this paper we describe the epidemiology of STEC in Australia using the latest available data.MethodsNational and state notifications data, as well as data on serotypes, hospitalizations, mortality and outbreaks were examined.ResultsFor the 11 year period 2000 to 2010, the overall annual Australian rate of all notified STEC illness was 0.4 cases per 100,000 per year. In total, there were 822 STEC infections notified in Australia over this period, with a low of 1 notification in the Australian Capital Territory (corresponding to a rate of 0.03 cases per 100,000/year) and a high of 413 notifications in South Australia (corresponding to a rate of 2.4 cases per 100,000/year), the state with the most comprehensive surveillance for STEC infection in the country. Nationally, 71.2% (504/708) of STEC infections underwent serotype testing between 2001 and 2009, and of these, 58.0% (225/388) were found to be O157 strains, with O111 (13.7%) and O26 (11.1%) strains also commonly associated with STEC infections. The notification rate for STEC O157 infections Australia wide between 2001-2009 was 0.12 cases per 100,000 per year. Over the same 9 year period there were 11 outbreaks caused by STEC, with these outbreaks generally being small in size and caused by a variety of serogroups. The overall annual rate of notified HUS in Australia between 2000 and 2010 was 0.07 cases per 100,000 per year. Both STEC infections and HUS cases showed a similar seasonal distribution, with a larger proportion of reported cases occurring in the summer months of December to February.ConclusionsSTEC infections in Australia have remained fairly steady over the past 11 years. Overall, the incidence and burden of disease due to STEC and HUS in Australia appears comparable or lower than similar developed countries.

Food subsidy programs and the health and nutritional status of disadvantaged families in high income countries: a systematic review.

BackgroundLess healthy diets are common in high income countries, although proportionally higher in those of low socio-economic status. Food subsidy programs are one strategy to promote healthy nutrition and to reduce socio-economic inequalities in health. This review summarises the evidence for the health and nutritional impacts of food subsidy programs among disadvantaged families from high income countries.MethodsRelevant studies reporting dietary intake or health outcomes were identified through systematic searching of electronic databases. Cochrane Public Health Group guidelines informed study selection and interpretation. A narrative synthesis was undertaken due to the limited number of studies and heterogeneity of study design and outcomes.ResultsFourteen studies were included, with most reporting on the Special Supplemental Nutrition Program for Women, Infants and Children in the USA. Food subsidy program participants, mostly pregnant or postnatal women, were shown to have 10–20% increased intake of targeted foods or nutrients. Evidence for the effectiveness of these programs for men or children was lacking. The main health outcome observed was a small but clinically relevant increase in mean birthweight (23–29g) in the two higher quality WIC studies.ConclusionsLimited high quality evidence of the impacts of food subsidy programs on the health and nutrition of adults and children in high income countries was identified. The improved intake of targeted nutrients and foods, such as fruit and vegetables, could potentially reduce the rate of non-communicable diseases in adults, if the changes in diet are sustained. Associated improvements in perinatal outcomes were limited and most evident in women who smoked during pregnancy. Thus, food subsidy programs for pregnant women and children should aim to focus on improving nutritional status in the longer term. Further prospective studies and economic analyses are needed to confirm the health benefits and justify the investment in food subsidy programs.

An outbreak of Salmonella Typhimurium 9 at a school camp linked to contamination of rainwater tanks

In March 2007, an outbreak of gastroenteritis was identified at a school camp in rural Victoria, Australia, affecting about half of a group of 55 students. A comprehensive investigation was initiated to identify the source. Twenty-seven attendees were found to have abdominal pain, diarrhoea and nausea (attack rate 49%). Of 11 faecal specimens tested all were positive for Salmonella Typhimurium definitive phage type 9 (DT9). Of four samples taken from the untreated private water supply, two were positive for DT9. Drinking water from containers filled from rainwater tanks [relative risk (RR) 3.2, P=0.039] and participation in two recreational activities - flying fox (RR 5.3, P=0.011), and beam-balance (RR 3.9, P=0.050) - were indicative of a link with illness. Environmental and epidemiological investigations suggested rainwater collection tanks contaminated with DT9 as being the cause of the outbreak. Increased use of rainwater tanks may heighten the risk of waterborne disease outbreaks unless appropriate preventative measures are undertaken.

Changes in bronchial hyperresponsiveness following high- and low-sulphite wine challenges in wine-sensitive asthmatic patients

Background Previous studies suggest that challenge of most wine‐sensitive asthmatic patients may not result in a reduction in forced expiratory volume in 1 s (FEV1).

Proportion of Illness Acquired by Foodborne Transmission for Nine Enteric Pathogens in Australia: An Expert Elicitation

BACKGROUND Estimates of the burden of illness acquired from food inform public health policy and prioritize interventions. A key component of such estimates is the proportion of illnesses that are acquired by foodborne transmission. In view of the shortage of requisite data, these proportions are commonly obtained through a process known as expert elicitation. We report findings from an elicitation process used to assess the importance of the foodborne transmission route for nine pathogens in Australia, circa 2010. MATERIALS AND METHODS Eleven experts were asked to estimate the proportion of illness acquired by five transmission routes: food, environmental, water, person, and zoonotic, together with a 90% certainty interval for foodborne transmission. Foodborne estimates and intervals from each expert were combined using both modified triangular and Program Evaluation and Review Technique (PERT) distributions, in @Risk version 6, to generate final distributions from which median estimates and 95% Credible Intervals (CrI) were calculated. RESULTS Shiga toxin-producing Escherichia coli (STEC) was the only pathogen believed to have an important zoonotic transmission route, while norovirus, hepatitis A virus, non-STEC pathogenic E. coli, and Shigella spp. were all thought to be primarily spread from person to person. Foodborne transmission was the main route for Clostridium perfringens (98%, CrI: 84-100), Listeria monocytogenes (98%, CrI: 86-100), nontyphoidal Salmonella spp. (72%, CrI: 50-87), and Campylobacter spp. (77%, CrI: 60-90). Foodborne estimates using the modified triangular distribution had wider CrI than these calculated using the PERT distribution. CONCLUSIONS Foodborne proportions for most pathogens in this study were the same or lower than those estimated circa 2000 in Australia, with the greatest decline for non-STEC pathogenic E. coli. Inclusion of certainty intervals from experts helps to quantify the precision of foodborne proportions. A decline in estimates of the foodborne proportion for common pathogens will influence final estimates of the burden of illness acquired from food.