Julian Crane

Purpose: Aotearoa New Zealand (NZ) homes are cold by international standards, with many failing to achieve temperatures recommended by WHO housing and health guidelines. Despite strong evidence of seasonal exacerbations in Chronic Obstructive Pulmonary Disease (COPD), there has been little examination of the effect of household warmth, or housing quality on COPD outcomes. The Warm Homes for Elder New Zealanders (WHEZ) study aimed to see if subsidising electricity costs would improve the health outcomes of older people with COPD. Previous analysis showed a modest, typically 2–10% dependent on prior usage, increase in electricity use among the subsidised households.

Patients and Methods: Participants aged over 55 with doctor-diagnosed COPD were recruited from three regional centres, and where possible their dwelling was insulated after enrolment. A single-blinded randomised controlled trial of the effect of an electricity voucher (NZ$500) on health care usage during winter was carried out in three locations across New Zealand. The primary outcome was exacerbations treated with antibiotics, and/or corticosteroids. The Clinical Trial Registration is NCT01627418. Of the 520 participants assigned to a wave, partial or better data was achieved for 424; 215 of those were randomised to the early intervention group, and 209 to receive the intervention later.

Results: Despite the modest increase in energy use by study households, reported previously, there was no significant difference between study arms in the frequency of exacerbation of COPD (0.089, p=0.5875, 95% CI −1.406–1.584) nor hospitalisations. An exploratory analysis suggested a lower mortality among participants assigned to receive the intervention first (OR 0.310, p=0.0175, 95% CI 0.118–0.815).

Conclusion: This study showed little effect of winter electricity vouchers on exacerbations of COPD. However, such vouchers increased energy use and may have reduced overall mortality. A larger study, particularly with susceptible subpopulations, is recommended to examine this mortality impact further.

Background: Various observational studies have suggested that infants and young children who regularly sleep in synthetic bedding materials are more likely to experience wheezing and asthma, while children who use feather duvets and/or feather pillows are less likely to wheeze.

Methods: In Wellington, New Zealand, we conducted a three-armed, parallel, randomised trial of 460 infants who were assigned to use different bedding materials: synthetic, wool or feather bedding in the form of sleepsacks from 3 months of age to 2 years of age to test the hypothesis that children exposed to feather materials are less likely to develop wheezing. Pregnant women were recruited before birth. Parents were unaware of the primary research hypothesis and were told this was a study of child warmth and wheezing. We have reported wheezing (parental and GP), a variety of respiratory health parameters and atopic status at 2 years.

Results: One hundred and forty-seven infants received a synthetic sleepsack, 150 wool and 144 feather. We have found no significant differences in reported or doctor-diagnosed wheezing or other respiratory health measures by bedding material used. For frequency of wheezing presentation at GP surgery, there was a significant increased rate for children using feather materials compared to synthetic, relative rate 2.00 (95% CI: 1.14, 3.52).

Conclusion: This study does not support earlier observational studies that suggest higher rates of wheezing for children using synthetic bedding or lower rates for feather materials, at least for early childhood wheezing. Our study suggests that the explanation for the observational study findings may lie in selection bias, where the parents of at-risk children avoid feather bedding materials.

To observe upper respiratory tract infection (URTI) symptoms, rhinovirus levels and compliance with daily carrageenan nasal spray. 102 adults were randomized to carrageenan or saline placebo three times daily for 8 weeks and URTI symptoms were recorded. A control group (n = 42) only recorded URTI symptoms. Participants collected nasal swabs when symptomatic. Regular daily carrageenan prophylaxis resulted in consistent but nonsignificant reductions in URTI symptoms versus the placebo group. Saline placebo decreased and increased some cold symptoms compared with no treatment. Daily prophylactic administration of antiviral carrageenan may not significantly reduce URTI symptoms. Due to low compliance, use in a population with specific reasons to avoid URTIs may be more appropriate. Disease-specific outcomes may be more useful than symptom reporting.

Neural and remodeling mechanisms may play a role in asthma, particularly noneosinophilic asthma (NEA). To assess sputum mediators associated with neural, remodeling, and inflammatory mechanisms in eosinophilic asthma (EA), NEA, and participants without asthma. A total of 111 participants with and 62 without asthma (14-21 years old) underwent sputum induction, exhaled nitric oxide, atopy, and spirometry tests. There were 24 mediators measured in sputum using enzyme-linked immunosorbent assay or bead array. Eosinophilic asthma (n = 52) and NEA (n = 59) were defined using a sputum eosinophil level cut-point of greater than or equal to 2.5%. Elevated levels of nociceptin (median: 39.1 vs 22.4 ng/mL, P = .03), periostin (33.8 vs 9.4 ng/mL, P = .01), and ECP; (220.1 vs 83.7 ng/mL, P = .03) were found in patients with asthma compared with those without asthma. Nociceptin was elevated in EA (54.8 vs 22.4 ng/mL, P = .02) compared with participants without asthma. Eosinophilic asthma had higher levels of inflammatory mediators (ECP: 495.5 vs 100.3 ng/mL, P ≤ .01; interleukin-1β: 285.3 vs 209.3 pg/mL, P = .03; histamine: 5805.0 vs 3172.5 pg/mL, P < .01) and remodeling mediators (VEGF-A); 3.3 vs 2.5 ng/mL, P = .03; periostin: 47.7 vs 22.1 ng/mL, P = .04) than NEA. Whereas macrophages were associated with neural mediators, for example, neurokinin A (r = 0.27, P = .01) and nociceptin (r = 0.30, P = .02), granulocytes were associated with inflammatory and remodeling mediators (eg, ECP and VEGF-A correlated with neutrophils (r = 0.53 and r = 0.33, respectively, P < .01) and eosinophils (r = 0.53 and r = 0.29 respectively, P ≤ .01). Elevated levels of nociceptin and inflammatory and remodeling markers were found in EA, but no evidence for neural and remodeling pathways was found in NEA. Neural and remodeling mechanisms seem to coexist with inflammation.

Background Group A streptococcal (GAS) infections can trigger an immune-mediated response resulting in acute rheumatic fever (ARF). The role of social and environmental risk factors for GAS pharyngitis and skin infections are not well understood. This study aimed to identify factors associated with GAS pharyngitis and skin infections, and to determine if these are the same as those for ARF. Methods A case-control study, including 733 children aged 5-14 years, was undertaken between March 2018 and October 2019 in Auckland, New Zealand. Healthy controls (n =190) and symptomatic cases including GAS pharyngitis (n = 210), GAS seronegative carriers (n = 182), and GAS skin infections (n = 151) were recruited. Trained interviewers administered a comprehensive, pre-tested, face-to-face questionnaire. Findings Multivariable analysis identified strong associations between barriers to accessing primary healthcare and having GAS pharyngitis (adjusted OR 3 center dot 3; 95% CI 1 center dot 8-6 center dot 0), GAS carriage (aOR 2 center dot 9; 95% CI 1 center dot 5-6 center dot 0) or a GAS skin infection (aOR 3 center dot 5; 95% CI 1 center dot 6-7 center dot 6). Children who had GAS skin infections were more likely than all other groups to report living in a crowded home (aOR 1 center dot 9; 95% CI 1 center dot 0-3 center dot 4), have Maori or Pacific grandparents (aOR 3 center dot 0; 95% CI 1 center dot 2-7 center dot 6), a family history of ARF (aOR 2 center dot 2; 95% CI 1 center dot 1-4 center dot 3), or having a previous diagnosis of eczema (aOR 3 center dot 9; 95% CI 2 center dot 2-6 center dot 9). Interpretation Reducing barriers to accessing primary healthcare (including financial restrictions, the inability to book an appointment, lack of transport, and lack of childcare for other children) to treat GAS pharyngitis and skin infections could potentially reduce these infections and lead to a reduction in their sequelae, including ARF. These strategies should be co-designed and culturally appropriate for the communities being served and carefully evaluated. Copyright (c) 2022 The Author(s). Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)

To assess whether retrofitting home insulation can reduce the risk of respiratory disease incidence and exacerbation, a retrospective cohort study was undertaken using linked data from a national intervention program. The study population was made up of 1 004 795 residents from 205 001 New Zealand houses that received an insulation subsidy though a national Energy Efficiency and Conservation Authority program. A difference-in-difference model compared changes in the number of prescriptions dispensed for respiratory illness post- insulation to a control population over the same timeframe. New prescribing of chronic respiratory disease medication at follow-up was used to compare incidence risk ratios between intervention and control groups. Chronic respiratory disease incidence was significantly lower in the intervention group at follow-up: odds ratio 0.90 (95% CI: 0.86-0.94). There was also a 4% reduction in medication dispensed for treating exacerbations of chronic respiratory disease symptoms in the intervention group compared with the control group: relative rate ratio (RRR) 0.96 (95% CI: 0.96-0.97). There was no change in medication dispensed to prevent symptoms of chronic respiratory disease RRR: 1,00 (95% CI: 0.99-1.00). These findings support home insulation interventions as a means of improving respiratory health outcomes.

The World Health Organization (WHO) recommends minimum indoor temperatures of 18 °C to maintain health. In a study of 152 children's bedrooms in Wellington, New Zealand we aimed to establish the costs of following WHO advice, using standard heaters over eight weeks of autumn to spring to investigate household factors and heating behaviours that significantly increase heating costs. During the heating intervention a mean children's bedroom temperature of 20 °C (range of 17–23 °C) was achieved, over a mean period of 12.2 h per night, using on average 6.33 kWh per night. Five factors significantly affected energy use: keeping children's bedroom doors fully open, having three or more intervention weeks in mid-winter, presence of mould, housing built pre-1978, and the bedroom having two or more exterior walls. These data have important implications for the New Zealand Winter Energy Payment (WEP) policy, supporting low income households. Based on figures from this study, the projected cost to heat one child's bedroom (NZ$58 per month) equates to 46% of the 2021 WEP. The current WEP is insufficient to cover the costs of heating living areas and more than one child's bedroom and should be adjusted for number of children and climatic region. •- This paper describes a heating intervention study undertaken in New Zealand.•- Heating a child's bedroom to ∼20 °C all night in winter uses 6.33 kWh in Wellington.•- The current Winter Energy Payment is insufficient to heat multiple bedrooms.

Acute respiratory infections (ARIs) are a major cause of morbidity among children. Respiratory viruses are commonly detected in both symptomatic and asymptomatic periods. The rates of infection and community epidemiology of respiratory viruses in healthy children needs further definition to assist interpretation of molecular diagnostic assays in this population. Children otherwise healthy aged 1 to 8 years were prospectively enrolled in the study during two consecutive winters, when ARIs peak in New Zealand. Parents completed a daily symptom diary for 8 weeks, during which time they collected a nasal swab from the child for each clinical ARI episode. A further nasal swab was collected by research staff during a clinic visit at the conclusion of the study. All samples were tested for 15 respiratory viruses commonly causing ARI using molecular multiplex polymerase chain reaction assays. There were 575 ARIs identified from 301 children completing the study, at a rate of 1.04 per child‐month. Swabs collected during an ARI were positive for a respiratory virus in 76.8% (307 of 400), compared with 37.3% (79 of 212) of swabs collected during asymptomatic periods. The most common viruses detected were human rhinovirus, coronavirus, parainfluenza viruses, influenzavirus, respiratory syncytial virus, and human metapneumovirus. All of these were significantly more likely to be detected during ARIs than asymptomatic periods. Parent‐administered surveillance is a useful mechanism for understanding infectious disease in healthy children in the community. Interpretation of molecular diagnostic assays for viruses must be informed by understanding of local rates of asymptomatic infection by such viruses. Highlight During winter, children experienced acute respiratory infections at a rate of 1.04/month. A virus was detected in 76.8% of acute respiratory infections. Specific viruses are more likely to be associated with respiratory symptoms.