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PubMed1995

Sudden infant death syndrome in New Zealand: are risk scores useful? New Zealand National Cot Death Study Group.

STUDY OBJECTIVE: To evaluate the Christchurch, Invercargill, Dunedin (CID) and Oxford record linkage study (ORLS) risk scores in five regions of New Zealand and examine the effect of risk factors for sudden infant death syndrome (SIDS), such as prone sleeping position, maternal smoking, breast feeding, measures of illness, the use of antenatal classes, community health care, and medical services on a high and low risk group delineated by the CID score. DESIGN: This was a case-control study of infants dying of SIDS. SETTING: Both the cases and controls were born in one of five health districts in New Zealand and their parents were interviewed between 1 November 1987 and 31 October 1990. PARTICIPANTS: The cases were 485 infants who died of SIDS. The controls were a random sample drawn from the same five regions in which the cases were born, chosen so that their age on the day on which they were interviewed was similar to the age at death of the cases. Risk scores were calculated for 387 case and 1579 controls. MEASUREMENTS AND MAIN RESULTS: Using the recommended cut off points the sensitivity and specificity of the CID and ORLS were found to be similar to those described for other samples. The differences among the regions were significant. There was, however, no evidence that the association between SIDS and the risk factors considered was different in the high and low risk groups delineated by the CID score. The relative attributable risk for smoking was 32.3% in the high risk group. The excess risk that could be attributed to a different prevalence of any of the other risk factors in the high risk group was small when compared with the low risk group. CONCLUSIONS: Health care resources should be spent on promoting and evaluating good child care practices for all, rather than identifying and promoting special interventions for those in the high risk category.

Breast Feeding↗
PubMed2002

Nutrition labelling: perspectives of a bi-national agency for Australia and New Zealand.

Australia New Zealand Food Authority (ANZFA) is a bi-national government agency forming a partnership between all of Australia's States and Territories and the New Zealand government. Australia New Zealand Food Authority employs scientific, legal policy, communication and administrative staff in our Australia and New Zealand offices. Prior to 1991 each of Australia's States and Territories had their own food standards; however, in 1991 Commonwealth legislation was introduced to consolidate responsibility for developing food standards in one specialist agency and to ensure the uniformity of Standards across all States and Territories in Australia. This was extended to New Zealand in 1995 when we became a bi-national agency following the signing of a Treaty between Australia and New Zealand to develop joint food standards for both countries. Australia New Zealand Food Authority's objectives in setting food standards are to: protect public health and safety; provide adequate information to enable consumers to make informed choices; and prevent misleading or deceptive conduct. Health Ministers have recently approved a new Joint Food Standards Code for Australia and New Zealand. This is the result of over 6 year's work and many rounds of public consultation. The new Code has had extensive input from government agencies, industry and consumers. In drafting the new code our emphasis has been on making decisions based on sound science and the most up-to-date information available. We also recognized the need for Standards to be practical in not imposing unnecessary costs on food manufacturers with an inevitable flow on effect to consumer prices. The Joint Code will replace both the existing Australian Food Standards Code and the New Zealand Food Regulations after a 2-year transition period. During the development of the Joint Code a wide range of matters were considered in relation to labelling. Amongst these were consumer needs, costs to industry, voluntary versus mandatory, enforcement issues, relationship to advertising and exemptions. A number of features of the new Code relate specifically to labelling and include: warning and advisory statements; ingredients lists; date marking; directions for use and storage; nutrition information; legibility requirements; and percentage labelling. One of the key features of the Joint Code is the requirement for most packaged foods to bear a nutrition information panel (NIP). Information must be presented on the amount of fat, saturated fat, protein, energy, carbohydrates, sugars and sodium. For the majority of foods the label is the first and only source of information regarding the nutritional content of food purchased. Mandatory nutrition labelling will ensure that consumers are provided with key nutritional information about foods. Single ingredient produce such as fruit and vegetables, and some other foods such as spices, tea and coffee will be exempt. The new requirements will give consumers more nutritional information to allow product comparison. All products will be required to provide information on these nutrients on both a per 100 g basis and in terms of an average serving. In addition to the mandatory nutrient declarations NIP are also required to carry additional data for any substance for which a nutrition claim is made. During the 2-year transition period to December 2002 ANZFA will be working with industry, enforcement agencies and consumers to help to ensure that there is a smooth transition to the Joint Food Standards Code.

Australia↗
PubMed2005

Quantitative estimates of work-related death, disease and injury in New Zealand.

OBJECTIVES: New Zealand lacks comprehensive statistics on work-related injury and illness, and the impact of adverse work conditions on health is therefore not known. The objective of this study was to make quantitative estimates of the annual number of deaths from work-related disease and injury in New Zealand, as well as estimate the number of incident cases of work-related disease and injury. METHODS: Wherever possible, specific data for New Zealand were used, but, where adequate national data were lacking, a combination of New Zealand data and extrapolations from other countries was used. For work-related injury mortality and incidence, published studies and reports of the New Zealand Accident Compensation Corporation were primarily used. For work-related disease mortality, the likely population attributable fractions from overseas studies were mainly used, together with mortality data from New Zealand. For work-related disease incidence, both approaches were used. RESULTS: In New Zealand about 700-1000 deaths were estimated to occur annually from work-related disease and about 100 deaths from work-related injury. About 17 000-20 000 new cases of work-related disease occur annually and about 200 000 work-related accidents result in claims made to the New Zealand Accident Compensation Corporation. CONCLUSIONS: Despite their imprecision, these conservative estimates indicate the burden of work-related death, disease, and injury in New Zealand. The estimates by gender, industry, and disease types provide useful information for policy priorities.

Accidents, Occupational↗
PubMed2003

Genetic epidemiology of alpha-1 antitrypsin deficiency in North America and Australia/New Zealand: Australia, Canada, New Zealand and the United States of America.

Alpha-1-antitrypsin deficiency (AAT deficiency) is one of the most common serious hereditary disorders in the world, as its affects all major racial subgroups worldwide, and there are an estimated 120.5 million carriers and deficient subjects worldwide. This genetic disease is related to susceptibility for development of jaundice in infants, liver disease in children and adults and pulmonary emphysema in adults. Moreover, AAT deficiency carrier phenotypes (PiMS and PiMZ) and deficiency allele phenotypes (PiSS, PiSZ and PiZZ) are suspected to predispose subjects to a variety of other adverse health effects. Because there is a limited database on the number of individuals affected by this disease worldwide, we have collected data on control cohorts in genetic epidemiological studies published on case-control studies in the peer-reviewed literature worldwide. Based on these data, we estimated the numbers of carriers and deficiency allele combinations for the two most common defective alleles, namely PiS and PiZ in 58 countries worldwide. The present paper focuses on the distribution of the PiS and PiZ deficiency alleles in Australia, Canada, New Zealand and the United States of America. A total of 31,042,232 individuals at risk for adverse health effects have been calculated in these four countries: 2,144,158 in Australia, 3,258,564 in Canada, 430,922 in New Zealand and 24,909,548 in the United States of America. The prevalences for all five phenotypic classes of AAT deficiency in each of these countries is as follows: Australia 1 out of 8.9, Canada 1 out of 9.8, New Zealand 1 out of 8.5 and the United States of America 1 out of 11.3. The geographical distribution of individual control cohorts and estimates of the numbers of carriers and deficiency allele phenotypes in each of these four countries are given in individual tables.

Australia↗
PubMed1995

An attempt to estimate the incidence of cervical dysplasia in a group of New Zealand women using contraception. The New Zealand Contraception and Health Study Group.

We attempted to estimate incidence rates of cervical dysplasia and carcinoma in a cohort of 7,199 New Zealand women using contraception. The cohort was followed prospectively with periodic cervical smears, intended to be annual, over a 6-year period. The principal outcome investigated was a diagnosis of cervical dysplasia of any degree, from mild to severe dysplasia and including carcinoma in situ or invasive carcinoma, made cytologically by a central study laboratory and confirmed by histology or deoxyribonucleic acid (DNA) evaluation. These diagnoses are jointly referred to as "dysplasia." Two successive negative (nondysplastic) smears were required before a woman was considered eligible for the analysis of incidence. Even after these two negative smears, the estimated "incidence" of dysplasia declined markedly in each of the 5 years of the study, particularly among women who provided negative smears in each prior year. This suggests that prevalent cases were being diagnosed even after five or more negative smears. Assuming that nearly all of the prevalent cases were removed after five negative smears, our estimate of the annual incidence of cervical dysplasia in this population during this time period would be of the order of 5 per 1,000 per year. We conclude that the sensitivity of cervical testing for identifying cervical dysplasia is quite low in this population but is consistent with values reported from some other populations. Age at first intercourse, age at first pregnancy, number of sex partners, and current cigarette smoking were strongly associated with risk of dysplasia. Our data are equivocal on the question of whether age at first intercourse is a risk factor independently of the closely associated variable, number of sex partners.

Adult↗
PubMed1977

Initial experience with prazosin in New Zealand. A multicentre report. New Zealand Hypertension Study Group.

Data are presented on 282 patients who began taking prazosin before March, 1975, and whose progress was followed until March, 1976. The following conclusions can be drawn. (i) Prazosin is an effective and useful antihypertensive agent, best used with a diuretic and a beta-blocker. (ii) For patients with suspected or definite coronary artery disease, prazosin should not be used without a beta-blocker. (iii) In patients suspected of having incipient heart failure, prazosin should not be used without a diuretic, and the latter should be given first. (iv) many patients have little or no rise in heart rate with prazosin. However, patients with sinus tachycardia or a history of arrhythmias should preferably not be treated with prazosin. (v) The initial dose should be kept small (0-25 to 0-5 mg). Subsequent increments should also be small, not more than 2 mg/day. (vi) If prazosin is added to a regimen containing an adrenergic neurone-blocking drug, the dose of the latter should first be reduced. (vii) Prazosin should not, in the meantime, be used concomitantly with a phenothiazine, as the combination appears to be capable of causing agitation and confusion. (viii) There seems to be no long-term toxicity.

Adult↗
PubMed2006

A new cercaria and metacercaria of Acanthoparyphium (Echinostomatidae) found in an intertidal snail Zeacumantus subcarinatus (Batillaridae) from New Zealand.

A new 23-collar-spined cercaria and metacercaria are described from intertidal molluscs of the coast of New Zealand. The new cercaria found emerging from the mud snails Zeacumantus subcarinatus (Sowerby) (Prosobranchia: Batillariidae) is characterized mainly by the number and arrangement of the cephalic glands, the size of the suckers, and the size and number of the collar spines. The cercaria encysts in the cockle Austrovenus stutchburyi (Wood) (Bivalvia: Veneridae) which lives in sympatry with the first intermediate host throughout New Zealand. Laboratory infections of cockles by cercariae from naturally infected snails resulted in metacercariae identical to those found in naturally infected cockles. The main features of the cercaria and metacercaria are the presence of a reniform collar with 23 spines, two pairs of small cephalic glands at the oral sucker level, another two pairs of much longer ones posterior to the pharynx, and the excretory vesicle Y-shaped with the main collecting canals extending to the anterior level of the ventral sucker. Each of the main collecting canals had 10-11 pairs of bilateral diverticula between the anterior edge of the ventral sucker and anterior body end. A brief discussion of its possible life cycle and ecology is also provided.

Animals↗
PubMed2005

Reducing health disparities through primary care reform: the New Zealand experiment.

New Zealand experiences significant health disparities related to both ethnicity and deprivation; the average life expectancy for Maori New Zealanders is 9 years less than for other New Zealanders. The government recently introduced a set of primary care reforms aimed at improving health and reducing disparities by reducing co-payments, moving from fee-for-service to capitation, promoting population health management and developing a not for profit infrastructure with community involvement to deliver primary care. Funding for primary care visits will increase by some 43% over 3 years. This paper reviews policy documents and enrollment and payment data for the first 15 months to assess the likely impact on health disparities. The policy has been successfully introduced; over half the New Zealand population (of four million) enrolled in new Primary Health Organizations within 15 months. Over 400,000 people (half of them in vulnerable groups) gained improved access to primary care subsidies in the first 15 months. The combined effect of new payment rules and the deprived nature of the minority populations was that the average per person payment to PHOs on behalf of Maori and Pacific enrollees was more than 70% greater than the per person amount for other ethnicities for the period. The policy is consistent with the principles of the Alma Alta Declaration. Barriers to successful implementation include the risk of middle class capture of the additional funding; the risk that co-payments are not low enough to improve access for the poor; PHO inexperience; and the small size of many PHOs. Transitional equity and efficiency issues with the use of aggregate population characteristics to target higher subsidies are being ameliorated by the introduction of low cost access based on age. A tension between the twin policy goals of low cost access for all, and very low cost access for the most vulnerable populations is identified as a continuing and unresolved policy issue.

Community Health Centers↗
PubMed1990

Cancer incidence in New Zealand born residents of New South Wales.

Cancer incidence in New Zealand born residents of New South Wales (NSW) has been compared with that in the Australian born population using data from the NSW Central Cancer Registry for the period 1972-84. Indirectly age-standardised incidence ratios (SIR) showed that New Zealand born women living in NSW had higher rates of cancer at all sites combined (SIR = 112) and a significant excess of colorectal cancer (SIR = 126). Although overall cancer rates were similar in men born in New Zealand to those in the Australian born men, the New Zealanders had a significantly higher risk of colorectal (SIR = 124) and testicular cancer (SIR = 227), cancers which are more common in New Zealand than in Australia. While the SIRs for lung cancer in men and melanoma of skin in both sexes were low, no cancer was significantly less common in New Zealand born residents of NSW than in the Australian born.

Colonic Neoplasms↗
PubMed2004

Separation of the New Zealand Black genetic contribution to lupus from New Zealand Black determined expansions of marginal zone B and B1a cells.

The F(1) hybrid of New Zealand Black (NZB) and New Zealand White (NZW) mice develop an autoimmune disease similar to human systemic lupus erythematosus. Because NZB and (NZB x NZW)F(1) mice manifest expansions of marginal zone (MZ) B and B1a cells, it has been postulated that these B cell abnormalities are central to the NZB genetic contribution to lupus. Our previous studies have shown that a major NZB contribution comes from the Nba2 locus on chromosome 1. C57BL/6 (B6) mice congenic for Nba2 produce antinuclear Abs, and (B6.Nba2 x NZW)F(1) mice develop elevated autoantibodies and nephritis similar to (NZB x NZW)F(1) mice. We studied B cell populations of B6.Nba2 mice to better understand the mechanism by which Nba2 leads to disease. The results showed evidence of B cell activation early in life, including increased levels of serum IgM, CD69(+) B cells, and spontaneous IgM production in culture. However, B6.Nba2 compared with B6 mice had a decreased percentage of MZ B cells in spleen, and no increase of B1a cells in the spleen or peritoneum. Expansions of these B cell subsets were also absent in (B6.Nba2 x NZW)F(1) mice. Among the strains studied, B cell expression of beta(1) integrin correlated with differences in MZ B cell development. These results show that expansions of MZ B and B1a cells are not necessary for the NZB contribution to lupus and argue against a major role for these subsets in disease pathogenesis. The data also provide additional insight into how Nba2 contributes to lupus.

Animals↗
PubMed2005

Nitric oxide levels and ciliary beat frequency in indigenous New Zealand children.

New Zealand children's morbidity from respiratory disease is high. This study examines whether subclinical ciliary abnormalities underlie the increased prevalence of respiratory disease in indigenous New Zealand children. A prospective study enrolled a group of healthy children who were screened for respiratory disease by questionnaire and lung function. Skin-prick tests were performed to control for atopy. Exhaled and nasal NO was measured online by a single-breath technique using chemiluminescence. Ciliary specimens were obtained by nasal brushings for assessment of structure and function. The ciliary beat frequency (CBF) (median CBF, 12.5 Hz; range, 10.4-16.8 Hz) and NO values (median exhaled NO, 5.6 ppb; range, 2.3-87.7 ppb; median nasal NO, 403 ppb; range, 34-1,120 ppb) for healthy New Zealand European (n=58), Pacific Island (n=61), and Maori (n=16) children were comparable with levels reported internationally. No ethnic differences in NO, atopy, or CBF were demonstrated. Despite an apparently normal ciliary beat, the percentage of ciliary structural defects was 3 times higher than reported controls (9%; range, 3.6-31.3%), with no difference across ethnic groups. In conclusion, it is unlikely that subclinical ciliary abnormalities underlie the increased prevalence of respiratory disease in indigenous New Zealand children. The high percentage of secondary ciliary defects suggests ongoing environmental or infective damage.

Adolescent↗