Between 1944 and 1979 the McIntyre Mining Company and many other mine
operators in northern Ontario deliberately exposed their workers to McIntyre
powder, a form of powdered aluminium, for between 10 and 20 minutes each
day. They did so in good faith, aiming to protect the men from silicosis,
a severe lung disease caused by exposure to silicon dust.

However, many miners opposed the use of the powder and, as evidence
mounted that aluminium might affect the brain, their unions pressed the
Ontario Ministry of Labour to investigate. In 1979 a study by the ministry
found that evidence for the safety and effectiveness of the powder was insufficient,
and the companies stopped using it. Since then, the unions have pressed
for studies into the effects of the powder.

McIntyre powder was developed in the 1940s by scientists at the McIntyre
Research Foundation and the Banting Institute of the University of Toronto.
It was designed to bind with silicon dust, creating a stable and inert compound
that would not damage the lungs. ‘Animal studies were convincing, and chemically
it makes sense,’ said Rifat. ‘The problem is, how do you know how much is
needed, and what becomes of the excess?’

Rifat traced more than 1000 retired miners between the ages of 60 and
70. Of these 250 had either died or had left the area. Of the remainder,
673 agreed to participate in a study. Those who had worked in gold and uranium
mines had been exposed to the powder for between six months and 36 years.
The duration of exposure for each miner was documented in company records.
A group of miners from nickel and copper mines, where the powder was not
used, served as controls.

The researchers interviewed each man and asked them to complete three
different standard cognitive tests which measure, for example, short-term
memory. Overall, 13 per cent of the miners exposed to the powder showed
signs of cognitive impairment, compared with 5 per cent of the control group.

In men exposed for more than 20 years, the effect was more pronounced,
with one-fifth of the exposed group showing impairment. And there was a
clear dose-response effect, says Rifat: the longer the period of exposure,
the poorer the performance. Her analysis was adjusted for differences in
education and other factors, such as previous head injuries, that could
affect performance.

Rifat says this is the first clear evidence that occupational exposure
to aluminium can affect mental ability. But she stressed that the cognitive
tests merely measure behaviour and cannot make a specific medical diagnosis.
Announcing her results at a conference in Toronto, Rifat said she hopes
to do studies to determine the physiological cause for the defects.

Donald McLachlan, a colleague of Rifat and a leading researcher into
aluminium’s effects on the brain, said he had been trying for years to obtain
the data. ‘They were stonewalling us,’ he said. Finally, the Ontario Ministry
of Labour asked the mining companies to cooperate. A spokesman for the McIntyre
Research Foundation was not available for comment.

Norman Carriere, the health and safety coordinator for the Ontario district
of the United Steel Workers of America, which represents many Ontario miners,
says that the mining unions had opposed the use of the powder since the
1960s. They had argued that silicosis could instead be prevented by adequate
ventilation and respirators.

Canadian law bars workers from suing the companies they work for, but
the unions are now fighting to obtain compensation for those affected. Rifat,
however, says the companies should not be blamed. She points out that deaths
from silicosis declined steadily over the period. ‘But there is no way to
know if that was due to the powder or to improvements in ventilation and
other hygiene measures implemented during that period,’ she says. ‘We now
have evidence that it (the powder) caused harm, but at this point it’s impossible
to know if it was beneficial as well.’

For several years, researchers have had evidence that one form of Alzheimer’s
is linked to a defective gene on chromosome 21 (91av, Science,
4 March 1989). This inherited form of Alzheimer’s tends to affect relatively
young people under the age of 65, and accounts for a small minority of all
those with the disease. The new study suggests that there may be a second
inherited form that accounts for at least some of those developing the disease
in their eighties.

Allen Roses at Duke University Medical Center in Durham, North Carolina,
has studied 32 families where several members had developed Alzheimer’s
late in life. He announced his results at the Second International Conference
on Alzheimer’s Disease and Related Disorders in Toronto.

Roses found that sufferers tended to have two specific genetic ‘markers’
which their healthy relatives often lacked. Markers are DNA sequences pinpointed
on the genetic map; researchers identify them using a biochemical probe.
The more frequently the disease and a marker are inherited together, the
more likely it is that the defective gene lies nearby on the same chromosome.

In this case, the two markers are on the long arm of chromosome 19,
suggesting that the defect lies there, too. The link between the markers
and the disease is weak, but statistically significant. The next step is
to identify the gene itself and sequence it.

‘The data are good,’ said John Hardy from St Mary’s Hospital in London,
one of the key researchers to confirm a link between chromosome 21 and the
early-onset disease. Hardy was disappointed that a single gene could not
explain all inherited Alzheimer’s: ‘It’s not a result I like, but I can’t
argue against it.’

However, scientists still face a problem. Genetic studies of late-onset
Alzheimer’s are difficult because the disease affects people in their eighties
and nineties, and many of their relatives have already died of other causes.
So it is impossible to say which relatives might have developed Alzheimer’s
had they survived.

Many scientists at the conference thought that Alzheimer’s disease would
eventually be seen as the result of a complex interaction of genetic, cellular
and environmental factors.